Coprobacter

What was studied?

The human microbiome plays a vital role in human health, mediated by the gut-brain axis, with a large diversity of functions and physiological benefits. The dynamics and mechanisms of meditations on oral and gut microbiome modulations are not well understood. This study investigates the short-term modulations of the gut and oral microbiome during an Arhatic Yoga meditation retreat as well as on the role of microbiome in improving well-being through a possible gut-brain axis.

Who was studied?

A single-arm pilot clinical trial was conducted in a controlled environment during a 9-day intensive retreat of Arhatic Yoga meditation practices with vegetarian diet. Oral and fecal samples of 24 practitioners were collected at the start (Day0: T1), middle (Day3: T2), and end (Day9:T3) of the retreat. Targeted 16S rRNA gene amplicon sequencing was performed for both oral and gut samples. Functional pathway predictions was identified using phylogenetic investigation of communities by reconstruction of unobserved states (PICRUSt2). DESeq2 was used to identify the differential abundant taxa. Various statistical analyses were performed to assess the significant changes in the data.

What were the most important findings?

Our findings revealed that Arhatic Yoga meditation together with a vegetarian diet led to changes in the oral and gut microbiome profiles within the 9-day retreat. Oral microbiome profile showed a significant (p < 0.05) difference in the species richness and evenness at the end of study, while non-metric multidimensional scaling (NMDS) confirmed the shift in the gut microbiome profile of the practitioners by T2 timepoint, which was further supported by PERMANOVA analysis (p < 0.05). Health-benefiting microbes known to improve the gastrointestinal and gut-barrier functions, immune modulation, and gut-brain axis were enriched. Gut microbiome of both beginner and advanced Arhatic Yoga practitioners showed similar trends of convergence by the end of study. This implies a strong selection pressure by Arhatic Yoga meditation together with a vegetarian diet on the beneficial gut microbiome.

What are the greatest implications of this study?

This pilot study demonstrates that Arhatic Yoga meditation practices combined with a vegetarian diet during a short intensive retreat resulted in enrichment of known health-promoting microbes. Such microbial consortia may be developed for potential health benefits and used as probiotics to improve the gastrointestinal and immune systems, as well as functions mediated by the gut-brain axis.

What was studied?

This study aimed to explore the distinct characteristics of the gut microbiota in tuberculosis (TB) patients who experienced liver injury following anti-TB treatment compared with those who did not.

Who was studied?

We employed a nested case-control study design, recruiting newly diagnosed pulmonary TB patients at Tangshan Infectious Disease Hospital. Participants were categorized into the Antituberculosis Drug-Induced Liver Injury (ADLI) group and the Non-ADLI group based on the occurrence of liver injury after treatment. Both groups received identical anti-TB regimens. Stool samples were collected from patients who developed liver injury within 2-3 weeks of starting treatment, alongside matched controls during the same timeframe. The samples underwent 16S rDNA sequencing, and clinical data and blood samples were also collected for further analysis. At the same time, we constructed mouse models to explore the effects of different anti-tuberculosis drugs on gut microbiota.

What were the most important findings?

Following anti-TB treatment, we observed a decrease in microbial diversity and significant structural changes in the gut microbiota of TB patients (P < 0.05). At T1, the Non_ADLI_T1 group presented relatively high levels of Phascolarctobacterium, Anaerofustis and Mailhella. In contrast, the ADLI_ T1 group presented elevated levels of Bacteroides, Veillonella, Clavibacter, Corynebacterium, Anaerococcus, Gardnerella, Peptostreptococcus and Lautropia. At T2, the ADLI_T2 group presented increased levels of Enterococcus, Faecalibacterium, unclassified_f__Burkholderiaceae, Cardiobacterium, Ruminococcus_gnavus_group and Tyzzerella_4 than did the Non_ADLI_T2 group. Additionally, the ADLI_T2 group presented decreased levels of Prevotella_9, Akkermansia, Erysipelotrichaceae_UCG-003, Rubrobacter and norank_f__Desulfovibrionaceae than did the Non_ADLI_T2 group. In animal experiments, similar changes to those in the human population were observed in the mouse model compared to the control group. Any single anti-tuberculosis drug or two-drug combination or three-drug combination can cause dysbiosis of the mouse gut microbiota. The signature genera between groups are different and related to the type of anti-tuberculosis drug.

What are the greatest implications of this study?

Anti-tuberculosis treatment induces dysbiosis in the gut microbiota of TB patients. Notably, there are significant differences in microbiota characteristics between TB patients with and without liver injury at both onset and during treatment. There are some differences in the characteristics of bacterial flora in liver injury caused by different drugs.

What was studied?

A plant-focused, healthy dietary pattern, such as the Mediterranean diet enriched with dietary fiber, polyphenols, and polyunsaturated fats, is well known to positively influence the gut microbiota. Conversely, a processed diet high in saturated fats and sugars negatively impacts gut diversity, potentially leading to weight gain, insulin resistance, and chronic, low-grade inflammation. Despite this understanding, the mechanisms by which the Mediterranean diet impacts the gut microbiota and its associated health benefits remain unclear.

Who was studied?

This retrospective, observational study explored the relationships between Mediterranean dietary components-vegetables, fruits and nuts, legumes, whole grains, fish, meat, dairy, alcohol, saturated and unsaturated fats-and the gut microbiota in middle-aged adults enrolled in Alberta's Tomorrow Project, Canada. Diet was recorded using the Canadian Dietary History Questionnaire (CDHQ-II) and participants were classified into four quartiles based on a modified Mediterranean Diet Score. Blood and fecal samples were collected for metabolomics and 16S rRNA sequencing, respectively.

What were the most important findings?

Findings revealed that higher adherence to the Mediterranean diet was associated with increased alpha diversity and a greater abundance of beneficial fiber-degrading bacteria, including Prevotella, Parabacteroides, Clostridium XIVb, Coprobacter, and Turicibacter. Furthermore, participants who consumed more Mediterranean diet components exhibited higher concentrations of serum microbial metabolites including p-hydroxy hippuric acid and indole-acetaldehyde.

What are the greatest implications of this study?

Results demonstrate a pivotal role of the gut microbiota, via its metabolites in harnessing the health benefits of the Mediterranean diet, highlighting its potential to promote metabolic health and prevent chronic disease.

What was studied?

This study examined whether the intestinal microbiota differs between men and women who have coronary heart disease (CHD). The researchers compared microbiota composition in CHD patients against non-CVD controls, analyzing each sex separately. Intestinal bacteria were profiled using 16S metagenomic sequencing on the Illumina MiSeq platform, with data processed in Qiime2. The goal was to identify sex-specific microbial patterns tied to cardiovascular disease.

Who was studied?

The study drew on the CORDIOPREV clinical trial cohort, which included 837 men and 165 women with CHD. These CHD patients were compared against a reference group of 375 individuals without cardiovascular disease, consisting of 270 men and 105 women. In total, the analysis spanned over 1,300 participants across both sexes and disease status.

What were the most important findings?

Beta diversity, reflecting differences in microbial community composition, varied by sex, while alpha diversity (within-sample richness) remained similar between men and women. LEfSe analysis identified sex-specific alterations in the gut microbiota associated with CVD. Using random forest modeling, the researchers pinpointed seven bacterial taxa as key discriminators: g_UBA1819 (Ruminococcaceae), g_Bilophila, g_Subdoligranulum, g_Phascolarctobacterium, f_Barnesiellaceae, g_Ruminococcus, and an unidentified genus within Ruminococcaceae (Ruminococcaceae incertae sedis).

What are the greatest implications of this study?

These findings suggest that cardiovascular disease is linked to distinct microbial signatures depending on sex, rather than a single universal gut microbiota pattern. This implies that future microbiome-based research or risk assessment for CHD may need to account for sex as a variable rather than treating cohorts as uniform. The identified taxa, several from the Ruminococcaceae family and related groups, may serve as candidate markers warranting further investigation in sex-stratified cardiovascular studies.

What was studied?

Possible relationships between gut dysbiosis and breast cancer (BC) development and progression have been previously reported. However, the results of these metagenomics studies are inconsistent. Our study involved 88 patients diagnosed with breast cancer and 86 cancer-free control women. Participants were divided into groups based on their menopausal status. Fecal samples were collected from 47 and 41 pre- and postmenopausal newly diagnosed breast cancer patients and 51 and 35 pre- and postmenopausal controls, respectively. In this study, we performed shotgun metagenomic analyses to compare the gut microbial community between pre- and postmenopausal BC patients and the corresponding controls.

What were the most important findings?

Firstly, we identified 12, 64, 158, and 455 bacterial taxa on the taxonomy level of phyla, families, genera, and species, respectively. Insignificant differences of the Shannon index and β-diversity were found at the genus and species levels between pre- and postmenopausal controls; the differences concerned only the Chao index at the species level. No differences in α-diversity indexes were found between pre- and postmenopausal BC patients, although β-diversity differed these subgroups at the genus and species levels. Consistently, only the abundance of single taxa differed between pre- and postmenopausal controls and cases, while the abundances of 14 and 23 taxa differed or tended to differ between premenopausal cases and controls, and between postmenopausal cases and controls, respectively. There were similar differences in the distribution of enterotypes. Of 460 bacterial MetaCyc pathways discovered, no pathways differentiated pre- and postmenopausal controls or BC patients, while two and one pathways differentiated cases from controls in the pre- and postmenopausal subgroups, respectively.

What are the greatest implications of this study?

While our findings did not reveal an association of changes in the overall microbiota composition and selected taxa with the menopausal status in cases and controls, they confirmed differences of the gut microbiota between pre- and postmenopausal BC patients and the corresponding controls. However, these differences were less extensive than those described previously.

What was studied?

The study examined how peripheral neurons connected to the gastrointestinal tract influence the gut microbiome and gut physiology. Researchers activated choline acetyltransferase (ChAT)-expressing or tyrosine hydroxylase (TH)-expressing gut-associated neurons in mice. They then measured effects on intestinal microbial communities, microbial metabolites (including bile acid profiles), and host physiological responses using multi-omics approaches.

Who was studied?

The subjects were mice in which ChAT+ or TH+ gut-associated neurons were experimentally activated. The abstract does not give a specific sample size or strain detail, so no cohort numbers can be stated. This was an animal model study, not a human cohort, and it generated multi-omics datasets from these mice rather than drawing on a public metagenomic dataset.

What were the most important findings?

Activating either ChAT+ or TH+ neurons reshaped the structure of the intestinal microbiome, including changes to bile acid profiles and fungal colonization. Physiologically, activation of either neuron type increased fecal output, showing a shared downstream effect on gut transit. Only ChAT+ neuron activation additionally increased colonic contractility and produced diarrhea-like fluid secretion, indicating that these two neuronal subtypes act through distinct physiological pathways despite some overlapping effects.

What are the greatest implications of this study?

The findings show that distinct subsets of peripheral, gut-associated neurons can independently shape microbiome composition and gastrointestinal physiology without requiring signals from the brain. This suggests the enteric and peripheral nervous system directly sculpts microbial ecology, including bacterial and fungal populations and bile acid metabolism, rather than the microbiome being shaped only by diet or host genetics. Because different neuron subtypes produce different physiological outcomes (fecal output alone versus contractility and diarrhea-like secretion), this points to neuron-specific pathways as potential targets for understanding or treating GI motility and secretory disorders.

What was studied?

This study tested whether Parkinson's disease alters the periodontitis-associated oral microbiome. Researchers collected unstimulated saliva samples and stool samples and profiled microbial communities using next-generation sequencing of the 16S ribosomal RNA gene (V1-V3 regions). Clinical, periodontal, and neurological parameters were recorded, including the severity of Parkinson's disease motor dysfunction.

Who was studied?

Three groups were enrolled: patients with periodontitis and Parkinson's disease (PA+P), patients with periodontitis but without Parkinson's disease (P), and systemically and periodontally healthy individuals used as controls (HC). The abstract does not give exact group sizes. The PA+P group had mild to moderate motor dysfunction, and plaque scores were comparable between the PA+P and P groups, indicating similarly effective oral hygiene.

What were the most important findings?

Beta diversity in saliva differed significantly between HC and PA+P, between HC and P, and between P and PA+P groups, showing that both periodontitis and the presence of Parkinson's disease reshape the oral microbial community. Saliva and fecal microbial profiles were distinct from each other. Mycoplasma faucium, Tannerella forsythia, Parvimonas micra, and Saccharibacteria (TM7) were increased in the P group, while Prevotella pallens, Prevotella melaninogenica, and Neisseria multispecies were more abundant in the PA+P group. In fecal samples from the P group, Ruthenibacterium lactatiformans, Dialister succinatiphilus, Butyrivibrio crossotus, and Alloprevotella tannerae were detected.

What are the greatest implications of this study?

The findings support the hypothesis that Parkinson's disease is associated with a distinct periodontitis-related oral microbial signature, separate from periodontitis alone. Because oral and gut microbial profiles diverged between groups despite similar oral hygiene, the results suggest disease-associated shifts rather than simple hygiene differences drive these community changes. This points to the oral-gut microbiome axis as a potential area for further investigation in Parkinson's disease and periodontitis.

What was studied?

This study examined the early development of the human gut microbiome by comparing infants to their mothers and grandmothers within the same family lines. Researchers used a multi-omics approach combining metagenomics (16S rRNA gene and shotgun sequencing) with two independent metabolomics platforms, gas chromatography and capillary electrophoresis coupled to mass spectrometry. The goal was to characterize differences in microbial populations, function, and metabolite output across three generations.

Who was studied?

Fecal samples were collected from 200 individuals spanning three generations of the same families. This included infants aged 0 to 12 months (55% female, 45% male) along with their respective mothers and grandmothers. The design allowed direct comparison of gut microbiota and metabolome across a shared generational line.

What were the most important findings?

Infants showed markedly less diverse gut microbiota than their mothers and grandmothers, along with distinct microbial population and functional profiles. The infant metabolome also differed substantially from the adults, particularly in short- and branched-chain fatty acids. These metabolite shifts were linked to corresponding differences in bacterial populations between infants and elders.

What are the greatest implications of this study?

The findings offer biochemical insight into how the gut microbiome is shaped during infancy within a single family lineage. Because dysregulation of the gut microbiome at this early stage may contribute to disease later in life, understanding these generational differences could inform strategies to support healthy microbiome development in infants. The authors suggest this multi-omics approach could ultimately help improve childhood health outcomes.

What was studied?

This pilot prospective cohort study examined whether ethnicity influences gut microbiome dysbiosis in pregnancies complicated by gestational diabetes mellitus (GDM). The researchers also investigated whether diet and lifestyle modifications made after a GDM diagnosis could modulate the gut microbiome. Fecal samples were collected at two time points, 24 to 28 weeks and 36 to 40 weeks of gestation, and analyzed using targeted 16S rRNA gene-based amplicon sequencing. Statistical comparisons between groups used PERMANOVA, differential abundance testing used DeSeq2, and functional predictions were generated with PICRUSt2.

Who was studied?

The cohort included 53 women with GDM and 16 women without GDM, all residing in Singapore. Participants belonged to three Asian ethnic groups: Chinese, Malay, and Indian. This design allowed comparison of gut dysbiosis patterns both across GDM status and across ethnic background within the same population.

What were the most important findings?

Among women with GDM, gut microbiomes from the different ethnic groups shared common features rather than diverging by ethnicity. This suggests that GDM-related dysbiosis is a relatively consistent phenomenon across the Chinese, Malay, and Indian groups studied. The abstract indicates that ethnicity was not a major driver of the microbiome differences observed in these GDM pregnancies.

What are the greatest implications of this study?

If GDM-associated gut dysbiosis is largely independent of Asian ethnic background, microbiome-targeted strategies for GDM may generalize across these ethnic groups rather than needing ethnicity-specific approaches. This supports the idea that dietary and lifestyle interventions after a GDM diagnosis could be evaluated and applied similarly across diverse populations. As a pilot study, these findings point to the need for larger cohorts to confirm whether microbiome-based interventions can be standardized across ethnicities.

What was studied?

This study examined whether iron overload in thalassemia patients is linked to gut dysbiosis and cognitive impairment through the gut-brain axis. Researchers assessed iron burden, cognitive function, and both gut and blood microbiome composition across different blood-transfusion regimens. The goal was to determine whether specific microbial shifts track with iron accumulation and cognitive status in this population.

Who was studied?

Sixty participants were recruited, comprising healthy controls, transfusion-dependent thalassemia (TDT) patients, and non-transfusion-dependent thalassemia (NTDT) patients. TDT patients receive more frequent blood transfusions and, consistent with this, showed greater iron overload than NTDT patients. This design allowed comparisons of gut and blood microbiota across a spectrum of iron-overload severity within the same disease population.

What were the most important findings?

Most thalassemia patients developed gut dysbiosis, and about 25% developed minor cognitive impairment. Both TDT and NTDT groups showed increased Fusobacteriota and Verrucomicrobiota with decreased Fibrobacterota, and TDT patients had more abundant Verrucomicrobia, described as beneficial bacteria. Iron overload correlated with cognitive impairment, and increased Butyricimonas with decreased Paraclostridium was associated with higher cognitive function. No blood microbiota was detected, and blood bacterial profiles did not differ significantly between thalassemia patients and controls.

What are the greatest implications of this study?

The findings suggest that iron overload in thalassemia is associated with gut microbial imbalance that may relate to cognitive outcomes through the gut-brain axis. Specific gut taxa such as Butyricimonas and Paraclostridium emerge as candidate markers linked to cognitive function, while the blood compartment appears not to harbor a distinct microbiome signal in this context. This points to the gut, rather than blood, as the more relevant site for future investigation of microbiome-cognition relationships in iron-overloaded thalassemia patients.

What was studied?

This study examined the biogeography of the mucosa-associated microbiome (MAM) across different segments of the upper and lower gastrointestinal tract. Researchers compared microbial composition and bacterial load between patients with inflammatory bowel disease (IBD) and controls. They also looked at how the MAM related to proton pump inhibitor (PPI) use, gastrointestinal symptom severity, and symptom response to a standardised nutrient challenge. Microbial composition was assessed with 16S rRNA gene amplicon sequencing, and bacterial load was measured by qPCR on mucosal biopsies.

Who was studied?

The study included 59 controls without structural gastrointestinal abnormalities or symptoms, 44 patients with ulcerative colitis, and 31 patients with Crohn's disease. Biopsies were collected from multiple segments of both the upper and lower gastrointestinal tract in these participants. This gives a total of 134 individuals across three clinical groups.

What were the most important findings?

Microbial communities differed between the upper and lower gastrointestinal tract in their mucosal composition. IBD patients showed relative and absolute depletion of numerous genera known to produce butyrate and/or propionate compared with controls. The largest difference observed was depletion of Faecalibacterium in the lower gastrointestinal tract of patients with Crohn's disease. The abstract also indicates that PPI users showed a notable difference in the MAM, though the specific finding is cut off in the provided text.

What are the greatest implications of this study?

The findings suggest that loss of short-chain fatty acid producing bacteria, particularly Faecalibacterium, is a hallmark of mucosal dysbiosis in Crohn's disease at the site of tissue contact rather than only in stool. Mapping microbiome differences by gastrointestinal segment highlights that biogeography matters when interpreting mucosal microbiome studies in IBD. The association with PPI use also points to medication exposure as a factor that should be accounted for when characterizing the mucosa-associated microbiome in these patients.

What was studied?

Many human-targeted drugs alter the gut microbiome, leading to implications for host health. However, the mechanisms underlying these effects are not well known. Here we combined quantitative microbiome profiling, long-read metagenomics, stable isotope probing and single-cell chemical imaging to investigate the impact of two widely prescribed drugs on the gut microbiome. Physiologically relevant concentrations of entacapone, a treatment for Parkinson's disease, or loxapine succinate, used to treat schizophrenia, were incubated ex vivo with human faecal samples. Both drugs significantly impact microbial activity, more so than microbial abundance. Mechanistically, entacapone can complex and deplete available iron resulting in gut microbiome composition and function changes. Microbial growth can be rescued by replenishing levels of microbiota-accessible iron. Further, entacapone-induced iron starvation selected for iron-scavenging gut microbiome members encoding antimicrobial resistance and virulence genes. These findings reveal the impact of two under-investigated drugs on whole microbiomes and identify metal sequestration as a mechanism of drug-induced microbiome disturbance.

What was studied?

Constipation is a common symptom in maintenance hemodialysis patients and greatly affects the quality of survival of hemodialysis patients. Fecal microbiota transplantation and probiotics are feasible treatments for functional constipation, but there is still a gap in the research on the characteristics of gut flora in patients with maintenance hemodialysis combined with constipation. The aim of this study is to clarify the characteristics of the intestinal flora and its changes in maintenance hemodialysis patients with constipation.

Who was studied?

Fecal samples were collected from 45 participants, containing 15 in the maintenance hemodialysis constipation group,15 in the maintenance hemodialysis non-constipation group and 15 in the healthy control group. These samples were analyzed using 16S rRNA gene sequencing. The feature of the intestinal microbiome of maintenance hemodialysis constipation group and the microbiome differences among the three groups were elucidated by species annotation analysis, α-diversity analysis, β-diversity analysis, species difference analysis, and predictive functional analysis.

What were the most important findings?

The alpha diversity analysis indicated that maintenance hemodialysis constipation group was less diverse and homogeneous than maintenance hemodialysis non-constipation group and healthy control group. At the genus level, the top ten dominant genera in maintenance hemodialysis constipation group patients were Enterococcus, Escherichia-Shigella, Bacteroides, Streptococcus, Bifidobacterium, Ruminococcus_gnavus_group, Lachnospiraceae_unclassified, Faecalibacterium, Akkermansia and UCG-002. Compared with non-constipation group, the Enterococcus, Rhizobiales_unclassified, Filomicrobium, Eggerthella, Allobaculum, Prevotella_7, Gordonibacter, Mitochondria_unclassified, Lachnoanaerobaculum were significantly higher in constipation group (p<0.05). Compared with non-constipation group, the Kineothrix, Rhodopirellula, Weissella were significantly lower in constipation group (p<0.05). The predictive functional analysis revealed that compared with non-constipation group, constipation group was significantly enriched in pathways associated with pyruate metabolism, flavonoid biosynthesis.

What are the greatest implications of this study?

This study describes for the first time the intestinal microbiome characteristics of maintenance hemodialysis patients with constipation. The results of this study suggest that there is a difference in the intestinal flora between maintenance hemodialysis patients with constipation and maintenance hemodialysis patients without constipation.

What was studied?

The relationship between intestinal microbiome and colorectal cancer (CRC) progression is unclear. This study aims to identify the intestinal microbiome associated with CRC progression and construct predictive labels to support the accurate assessment and treatment of CRC.

Who was studied?

The 192 patients included in the study were divided into stage I-II and stage III-IV CRC patients according to the pathological stages, and preoperative stools were collected from both groups for 16S rDNA sequencing of the intestinal microbiota. Pearson correlation and Spearman correlation coefficient analysis were used to analyze the differential intestinal microbiome and the correlation with tumor microenvironment and to predict the functional pathway. XGBoost model (XGB) and Random Forest model (RF) were used to construct the microbiome-based signature. The total RNA extraction from 17 CRC tumor simples was used for transcriptome sequencing.

What were the most important findings?

The Simpson index of intestinal microbiome in stage III-IV CRC were significantly lower than those in stage I-II CRC. Proteus, Parabacteroides, Alistipes and Ruminococcus etc. are significantly enriched genus in feces of CRC patients with stage III-IV. ko00514: Other types of O - glycan biosynthesis pathway is relevant with CRC progression. Alistipes indistinctus was positively correlated with mast cells, immune activators IL-6 and IL6R, and GOBP_PROTEIN_FOLDING_IN_ENDOPLASMIC_RETICULUM dominantly. The Random Forest (RF) model and eXtreme Gradient Boosting (XGBoost) model constructed with 42 CRC progression-associated differential bacteria were effective in distinguishing CRC patients between stage I-II and stage III-IV.

What are the greatest implications of this study?

The abundance and diversity of intestinal microbiome may increase gradually with the occurrence and progression of CRC. Elevated fetal abundance of Proteus, Parabacteroides, Alistipes and Ruminococcus may contribute to CRC progression. Enhanced synthesis of O - glycans may result in CRC progression. Alistipes indistinctus may play a facilitated role in mast cell maturation by boosting IL-6 production. Alistipes indistinctus may work in the correct folding of endoplasmic reticulum proteins in CRC, reducing ER stress and prompting the survival and deterioration of CRC, which may owe to the enhanced PERK expression and activation of downstream UPR by Alistipes indistinctus. The CRC progression-associated differential intestinal microbiome identified in our study can be served as potential microbial markers for CRC staging prediction.

Who was studied?

A case-control study was conducted. Fecal microbiota was determined by 16S rDNA sequencing. The cases with CRC or adenoma were subclassified by gut microbiota enterotypes. Multivariate analyses were used to test associations between smoking and the odds of colorectal neoplasm subtypes. Mann-Whitney U tests were used to find differential genera, genes, and pathways between the subtypes.

What were the most important findings?

Included in the study were 130 CRC patients (type I: n=77; type II: n=53), 120 adenoma patients (type I: n=66; type II: n=54), and 130 healthy participants. Smoking increased the odds for type II tumors significantly (all p for trend <0.05) but not for type I tumors. The associations of smoking with increased odds of colorectal neoplasm significantly differed by gut microbiota enterotypes (p<0.05 for heterogeneity). An increase in carcinogenic bacteria (genus Escherichia shigella) and a decrease in probiotics (family Lachnospiraceae and Ruminococcaceae) in type II tumors may drive disease progression by upregulating oncogenic signaling pathways and inflammatory/oxidative stress response pathways, as well as protein phospholipase D1/2, cytochrome C, and prostaglandin-endoperoxide synthase 2 expression.

What are the greatest implications of this study?

Smoking was associated with a higher odds of type II colorectal neoplasms but not type I tumors, supporting a potential role for the gut microbiota in mediating the association between smoking and colorectal neoplasms.

What was studied?

This study investigated how rare, low-abundance bacterial phylotypes contribute to the microbial communities associated with urinary stone disease (USD), rather than focusing only on dominant, common taxa. The researchers conducted a meta-analysis of existing 16S rRNA sequencing datasets derived from kidney stone, stool, and urine samples. They separated bacterial taxa into rare and common groups based on the frequency and abundance of amplicon sequence variants, then compared how each group related to disease status across the three sample types. The aim was to clarify the distinct contribution of rare phylotypes to the gut, upper urinary, and lower urinary tract microbiomes in USD.

Who was studied?

The analysis drew on previously generated 16S rRNA datasets from participants with and without urinary stone disease, pooled across stone, stool, and urine sample types. The abstract does not specify exact participant numbers, ages, or geographic origin, so this appears to be a secondary meta-analysis of existing public or previously published cohort data rather than a newly recruited cohort. What can be said with confidence is that the population included both USD patients and comparison individuals without the disease.

What were the most important findings?

Consistent with prior work, the gut, upper urinary tract, and lower urinary tract microbiomes were each found to be distinct microbial communities. Rare phylotypes, those present at low frequency and abundance, comprised the majority of the taxa detected across kidney stone, stool, and urine samples. This indicates that the low-abundance portion of these communities is numerically dominant even though it is often overlooked in favor of common, high-abundance taxa. The abstract does not report findings related to Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism.

What are the greatest implications of this study?

The findings suggest that rare phylotypes deserve dedicated attention in future USD microbiome research, since they make up most of the taxonomic diversity across stone, stool, and urine niches. Because bacteriotherapies for urologic health are being developed based on microbiome composition, ignoring rare taxa could mean missing organisms relevant to disease onset or progression. This work supports a shift toward analytical approaches that explicitly separate rare from common phylotypes when characterizing the kidney stone, gut, and urinary tract microbiome relationship to USD.

What was studied?

This study examined whether the gut microbiome differs in young children with airway allergic disease compared with healthy children. Researchers used high-throughput metagenomic shotgun gene sequencing on fecal samples to characterize the gut microbiota at both the phylum and genus levels. The goal was to identify unique gut microbial features associated with allergic asthma and allergic rhinitis in children.

Who was studied?

The study included three groups of children: those with allergic asthma (n = 23), those with allergic rhinitis (n = 18), and healthy controls (n = 19). Fecal samples were collected from each child for shotgun metagenomic analysis. No further demographic details, such as age range or geographic location, are given in the abstract.

What were the most important findings?

Children with allergic asthma and allergic rhinitis showed increased gut microbial richness and diversity compared with healthy controls, with Simpson and Shannon diversity indices significantly elevated in the asthma group. Principal coordinates analysis showed that gut microbial community clustering in both allergic groups differed significantly from healthy controls, though asthma and rhinitis groups did not differ significantly from each other. At the phylum level, Firmicutes was enriched and Bacteroidetes was reduced in both allergic groups, while at the genus level Corynebacterium, Streptococcus, Dorea, Actinomyces, Bifidobacterium, Blautia, and Rothia were significantly enriched in the allergic children. The abstract does not mention Candida, fungi, yeast, or the mycobiome.

What are the greatest implications of this study?

The findings support a link between gut microbiome composition and airway allergic disease in children, suggesting the gut-lung axis may play a role in asthma and rhinitis development. The shared microbial alterations across asthma and rhinitis groups suggest a common underlying gut dysbiosis pattern rather than disease-specific signatures. These bacterial taxa could serve as candidate biomarkers or targets for future microbiome-directed strategies in pediatric airway allergic disease, pending further mechanistic and validation studies.

What was studied?

This study examined the gut microbiota and short-chain fatty acids (SCFAs) in children with constipated autism spectrum disorder (C-ASD). Researchers used an integrated approach combining 16S rRNA gene sequencing with gas chromatography-mass spectrometry-based metabolomics to characterize bacterial community composition and SCFA levels. The aim was to clarify the relationship between constipation, autism spectrum disorder, gut microbiota, and SCFAs, an area the authors describe as still debated.

Who was studied?

The study enrolled 80 Chinese children, divided into a constipated autism spectrum disorder (C-ASD) group of 40 children and a typically developing (TD) group of 40 children. Both groups were compared directly using the same 16S rRNA sequencing and metabolomics methods. The abstract does not provide further demographic details such as age range or sex distribution.

What were the most important findings?

Gut microbial community diversity, measured by the Observed, Chao1, and ACE indices, was significantly lower in the C-ASD group than in the TD group. Several taxa, including Ruminococcaceae_UCG_002, Phascolarctobacterium, Megamonas, Parabacteroides, Fusobacterium, and Prevotella species, were enriched in C-ASD children, while Anaerostipes, Lactobacillus, Ruminococcus_gnavus_group, and related taxa were enriched in TD children. Propionate levels were higher in the C-ASD group and were negatively correlated with other measured parameters, indicating altered SCFA metabolism alongside the shifted microbial community.

What are the greatest implications of this study?

The findings suggest that constipation in children with autism spectrum disorder is accompanied by a distinct, less diverse gut microbiota and altered short-chain fatty acid production, particularly elevated propionate. This supports the idea that gut microbial and metabolic changes are linked to gastrointestinal comorbidity in autism spectrum disorder rather than being incidental. These microbiota and SCFA signatures could inform future research into microbiome-targeted approaches for managing constipation in this population.

What was studied?

While dysbiosis within the intestinal ecosystem has been associated with functional constipation (FC), the mechanisms underlying the interactions between FC and the microbiome remain poorly elucidated. Recent investigations suggested that host microRNAs (miRNAs) can modulate bacterial growth and influence the composition of the gut microbiome. To explore the connection between gut microbiota and fecal miRNAs in FC patients, we initially employed 16S rRNA sequencing to assess the gut microbial landscape in 30 FC patients and 30 healthy controls (HCs). The α-diversity within the FC group exhibited some alterations, and the β-diversity significantly differed, signifying distinctive variations in gut microbiota composition between FC patients and HCs. Subsequently, we identified 44 differentially expressed (DE) miRNAs in feces from FC patients and HCs. Through correlation analysis between DE miRNAs and FC-associated microbiota, we detected an interaction involving nine DE miRNAs (miR-205-5p, miR-493-5p, miR-215-5p, miR-184, miR-378c, miR-335-5p, miR-514a-3p, miR-141-3p, and miR-34c-5p) with seven bacterial genera (Oscillibacter, Escherichia.Shigella, UCG.002, Lachnospiraceae_NK4A136_group, Lachnospiraceae_UCG.010, Eubacterium_ruminantium_group and Megamonas), as evidenced by a co-occurrence network. Further, a comprehensive panel of seven diagnostic biomarkers (Oscillibacter, Escherichia.Shigella, UCG.002, miR-205-5p, miR-493-5p, miR-215-5p, and Lachnospiraceae_NK4A136_group) demonstrated robust discriminatory capacity in predicting FC status when integrated into a random forest model (AUC = 0.832, 95% CI: 65.73-98.88). Microbiomes correlating with DE miRNAs exhibited enrichment in distinct predicted metabolic categories. Moreover, miRNAs correlated with FC-associated bacteria were found to be enriched in signaling pathways linked to colonic contractility, including Axon guidance, PI3K-Akt signaling pathway, MAPK signaling pathway, and Hippo signaling pathway. Our study offers a comprehensive insight into the global relationship between microbiota and fecal miRNAs in the context of FC, presenting potential targets for further experimental validation and therapeutic interventions.

What was studied?

Although the etiology of obsessive-compulsive disorder (OCD) is largely unknown, it is accepted that OCD is a complex disorder. There is a known bi-directional interaction between the gut microbiome and brain activity. Several authors have reported associations between changes in gut microbiota and neuropsychiatric disorders, including depression or autism. Furthermore, a pediatric-onset neuropsychiatric OCD-related syndrome occurs after streptococcal infection, which might indicate that exposure to certain microbes could be involved in OCD susceptibility. However, only one study has investigated the microbiome of OCD patients to date. We performed 16S ribosomal RNA gene-based metagenomic sequencing to analyze the stool and oropharyngeal microbiome composition of 32 OCD cases and 32 age and gender matched controls. We estimated different α- and β-diversity measures and performed LEfSe and Wilcoxon tests to assess differences in bacterial distribution. OCD stool samples showed a trend towards lower bacterial α-diversity, as well as an increase of the relative abundance of Rikenellaceae, particularly of the genus Alistipes, and lower relative abundance of Prevotellaceae, and two genera within the Lachnospiraceae: Agathobacer and Coprococcus. However, we did not observe a different Bacteroidetes to Firmicutes ratio between OCD cases and controls. Analysis of the oropharyngeal microbiome composition showed a lower Fusobacteria to Actinobacteria ratio in OCD cases. In conclusion, we observed an imbalance in the gut and oropharyngeal microbiomes of OCD cases, including, in stool, an increase of bacteria from the Rikenellaceae family, associated with gut inflammation, and a decrease of bacteria from the Coprococcus genus, associated with DOPAC synthesis.

What was studied?

This pilot study examined the gut microbiota of patients with brain tumors to determine whether benign and malignant tumors are associated with distinct microbial patterns. It compared microbial diversity and composition across benign meningioma, malignant glioma, and healthy control groups. The work builds on prior evidence linking gut microbiota to tumor growth, including malignant gliomas, via the brain-gut axis.

Who was studied?

The study included 32 patients with benign meningioma, 27 patients with malignant glioma, and 41 healthy individuals as controls. This gives a total pilot cohort of 100 participants across the three groups. No further demographic details are provided in the abstract.

What were the most important findings?

Brain tumor patients, both meningioma and glioma groups, showed lower gut microbial diversity than healthy controls, with no significant diversity difference between the two tumor groups. Microbial composition differed significantly between tumor patients and healthy participants. Meningioma patients had increased pathogenic bacteria such as Enterobacteriaceae, while glioma patients showed overrepresentation of carcinogenic bacteria including Fusobacterium and Akkermansia. Both benign and malignant tumor groups lacked SCFA-producing probiotic bacteria.

What are the greatest implications of this study?

The findings suggest that gut microbial alterations, including reduced diversity and loss of SCFA-producing bacteria, are associated with the presence of brain tumors generally, while specific taxa may distinguish benign from malignant disease. The identification of a candidate microbial biomarker panel, including Fusobacterium, Akkermansia, Escherichia/Shigella, Lachnospira, and Agathobacter, points toward potential non-invasive markers for differentiating tumor types. As a pilot study, these results support further investigation into the brain-gut axis as a factor in brain tumor pathology.

What was studied?

The colonic microbiome has been implicated in the pathogenesis of colorectal cancer (CRC) and intestinal microbiome alterations are not confined to the tumour. Since data on whether the microbiome normalises or remains altered after resection of CRC are conflicting, we studied the colonic microbiota of patients after resection of CRC. We profiled the microbiota using 16S rRNA gene amplicon sequencing in colonic biopsies from patients after resection of CRC (n = 63) in comparison with controls (n = 52), subjects with newly diagnosed CRC (n = 93) and polyps (i = 28). The colonic microbiota after surgical resection remained significantly different from that of controls in 65% of patients. Genus-level profiling and beta-diversity confirmed two distinct groups of patients after resection of CRC: one with an abnormal microbiota similar to that of patients with newly diagnosed CRC and another similar to non-CRC controls. Consumption levels of several dietary ingredients and cardiovascular drugs co-varied with differences in microbiota composition suggesting lifestyle factors may modulate differential microbiome trajectories after surgical resection. This study supports investigation of the colonic microbiota as a marker of risk for development of CRC.

What was studied?

This study examined the role of gut microbiota in two autoimmune thyroid conditions, Graves' disease (GD) and Hashimoto's thyroiditis (HT). Researchers used 16S sequencing to characterize fecal bacterial communities and chemiluminescence to measure thyroid function and autoantibodies (FT3, FT4, TSH, TRAb, TGAb, and TPOAb). Thyroid ultrasound was also used, and functional prediction of the microbiota was carried out using KEGG and COG analyses to explore possible mechanisms linking gut bacteria to disease.

Who was studied?

Seventy fecal samples were collected in total. These included 27 patients with Graves' disease, 27 patients with Hashimoto's thyroiditis, and 16 samples from healthy volunteers who served as controls.

What were the most important findings?

The overall structure of the gut microbiota in both the GD and HT groups differed significantly from that of the healthy control group. Proteobacteria and Actinobacteria were most abundant in the HT group, while both the GD and HT groups showed higher levels of Erysipelotrichia, Cyanobacteria, and Ruminococcus_2 and lower levels of Bacillaceae and Megamonas compared to controls. Functional analysis linked the ABC transporter pathway strongly to GD and HT, and COG analysis showed enrichment in carbohydrate transport and metabolism, but not amino acid transport and metabolism, in both patient groups.

What are the greatest implications of this study?

The findings suggest that gut microbiota alterations, particularly shifts in carbohydrate transport and metabolism pathways, may be mechanistically involved in the development of Graves' disease and Hashimoto's thyroiditis. This supports a role for the gut microbiome in autoimmune thyroid disease pathogenesis and points to specific bacterial taxa and metabolic pathways as potential targets for further mechanistic study. Because the abstract does not specify additional cohort details or long-term outcomes, further research is needed to confirm causality and clinical relevance.

What was studied?

This study examined the gut microbiome composition of children with Autism Spectrum Disorder (ASD) compared to neurotypical (NT) children. The researchers compiled ten publicly available amplicon and metagenomic sequencing datasets and combined them with new data from an internal cohort. All datasets were unified using standardized pre-processing methods and then analyzed together in a comprehensive meta-analysis. The goal was to identify reproducible ASD-specific microbiome signatures and to test associations between the microbiome and 52 clinical and demographic variables across multiple patient subsets.

Who was studied?

The analysis drew on children diagnosed with ASD and their neurotypical counterparts across ten publicly available sequencing datasets. It also incorporated a new internal cohort described as the largest ASD cohort compiled to date, though the abstract does not give an exact sample size. Subjects were further divided into subsets based on variables including age, sex, and bowel function to test for confounding effects.

What were the most important findings?

Differentially abundant taxa between ASD and NT children were found to depend heavily on age, sex, and bowel function, identifying these as major potential confounders in case-control ASD microbiome studies. Certain taxa, including the strains Bacteroides stercoris t__190463 and Clostridium M bolteae t__180407, and the species Granulicatella elegans and Massilioclostridium coli, only showed differential abundance between ASD and NT children after subjects with bowel dysfunction were excluded. Adjusting statistical models for age, sex, and bowel function changed which taxa appeared significantly associated with ASD, underscoring how much these variables shape reported microbiome signatures.

What are the greatest implications of this study?

The findings suggest that much of the prior inconsistency in reported ASD gut microbiome signatures may stem from unaccounted confounders such as age, sex, and bowel function rather than true absence of a signal. Future ASD microbiome research needs to systematically control for these variables to produce reproducible, comparable results across studies. The identification of specific taxa that emerge only after removing bowel dysfunction subjects points toward the possibility of more precise ASD patient subgroups defined by microbiome features.

What was studied?

This study examined the gut microbiota of patients with COVID-19 pneumonia using 16S rRNA gene sequencing performed on rectal swabs. Researchers compared microbial composition and diversity between patients treated in the intensive care unit (i-COVID19), patients treated in infectious disease wards (w-COVID19), and healthy controls (CTRL). The goal was to characterize how gut microbial communities differ across varying levels of COVID-19 disease severity.

Who was studied?

The study population consisted of patients hospitalized with COVID-19 pneumonia, divided into two groups by care setting: those admitted to the intensive care unit and those managed in infectious disease wards. These two patient groups were compared against a control group without COVID-19. The abstract does not report exact sample sizes, ages, or other demographic details for these cohorts.

What were the most important findings?

Patients in the ICU showed a decrease in the Chao1 index compared to both controls and ward patients, indicating lower microbial richness in the most severely ill patients, while the Shannon index showed no significant change. At the phylum level, ward patients showed an increase in Proteobacteria compared to controls. Fusobacteria and Spirochetes were both decreased relative to controls, with Spirochetes showing the greatest decrease in ICU patients specifically.

What are the greatest implications of this study?

The findings indicate that gut microbial communities shift in composition and richness according to COVID-19 disease severity, with the most pronounced changes occurring in critically ill ICU patients. These preliminary results suggest the gut microbiota may hold promising biomarkers for diagnosing COVID-19 and gauging disease severity. The authors note that validation in larger cohorts could support using microbiota profiles to help stratify patients by severity.

What was studied?

This study examined the gut microbiome of patients with Parkinson's disease (PD) using metagenomics paired with serum metabolomics. The researchers integrated these two data types through metabolic modeling and built a correlation network to connect microbial species with disease features. The goal was to clarify how gut bacteria relate to gastrointestinal dysfunction, an early and common nonmotor symptom of PD. Personalized, community-level metabolic models were used to estimate each patient's microbial metabolic contributions.

Who was studied?

The abstract describes patients with Parkinson's disease whose gut metagenomes and serum metabolomes were profiled, but it does not give an exact sample size or demographic breakdown. The analysis draws on individual-level, personalized metabolic models, indicating the cohort was studied at the level of single patients rather than pooled averages. Disease severity, gastrointestinal dysfunction, and age were all tracked as patient-level variables linked to microbial findings.

What were the most important findings?

The gut microbiome in PD patients showed an increased capacity to degrade mucin and host glycans, pointing to disruption of the gut mucus barrier. The integrative correlation network identified specific microbial species associated with disease severity, gastrointestinal dysfunction, and patient age. Personalized metabolic modeling further revealed that the gut microbiota contributes to folate deficiency and hyperhomocysteinemia observed in these patients. These results tie a specific microbial metabolic function, bacterial folate and homocysteine handling, to biochemical abnormalities already documented in PD.

What are the greatest implications of this study?

By linking microbial mucin degradation and altered folate/homocysteine metabolism to PD, the study suggests the gut microbiome may actively contribute to disease-associated gastrointestinal and metabolic disturbances, not just reflect them. The personalized metabolic modeling approach offers a template for uncovering how gut microbes shape PD pathophysiology in individual patients. This framework could help identify microbial targets tied to folate and homocysteine handling for further investigation in PD management.

What was studied?

This study examined the composition and functional potential of the gut microbiota in people with type 2 diabetes (T2D) across two distinct populations, Denmark and South India. The researchers used 16S ribosomal RNA gene amplicon sequencing on stool samples to compare the gut microbiota between countries and between people with and without T2D. A central goal was to determine whether any microbiome signature of T2D is universal across ethnicities and diets, or whether such signatures are instead country-specific. The study also looked at microbial associations with treatment using the anti-hyperglycemic drug metformin.

Who was studied?

The study population consisted of 279 Danish study participants and 294 Indian study participants, for a total of 573 people. Stool samples were collected from both cohorts and profiled using 16S rRNA gene amplicon sequencing. The abstract does not specify additional demographic details such as age or sex distribution within these two national cohorts.

What were the most important findings?

The gut microbiota differed measurably between the Danish and Indian populations, reflecting country-specific patterns in diversity and composition. Samples were stratified to look for both global (trans-ethnic) and country-specific microbial signatures associated with T2D and with metformin treatment. This approach allowed the researchers to separate microbial features that might be universal markers of T2D from those that are shaped by local diet or ethnic background. The abstract does not report specific taxa, effect sizes, or statistical values for these comparisons.

What are the greatest implications of this study?

By directly comparing two ethnically and geographically distinct populations, this study helps clarify whether gut microbiota changes linked to type 2 diabetes represent a truly universal signature or are instead dependent on diet and ethnic origin. This distinction matters for whether microbiome-based diagnostics or interventions for T2D could be applied globally or would need to be tailored to specific populations. Separating country-specific findings from trans-ethnic ones also helps prevent overgeneralizing microbiome associations discovered in a single population. The findings support continued large-scale, multi-population microbiome research as a foundation for any future universal T2D biomarkers.

What was studied?

This study examined the microbiological composition of the intestines of people with ulcerative colitis (UC) compared with healthy individuals. UC is an inflammatory disease affecting the colon and rectum, and the authors note that the role of intestinal microbiota in its pathogenesis has been incompletely characterized. The researchers used sequencing on the IonTorrent PGM system followed by data analysis to profile bacterial genera and species. They specifically framed the work as addressing a gap in comprehensive data on the microbial composition of UC patients in Russia.

Who was studied?

The study compared patients with ulcerative colitis to a control group of healthy individuals, with intestinal samples analyzed from both groups. The abstract does not give an exact number of participants, so no specific cohort size can be stated. The population is described as being from the Central European part of Russia, addressing what the authors describe as a lack of prior microbiological data on UC patients in that country.

What were the most important findings?

Sequencing revealed significant changes in bacterial genera and species in UC patients compared with controls. Several genera were significantly increased in UC patients, including Haemophilus, Olsenella, Prevotella, Cedecea, Peptostreptococcus, Faecalibacterium, Lachnospira, Negativibacillus, and Butyrivibrio. Species-level increases included Bacteroides coprocola, Phascolarctobacterium succinatutens, Dialister succinatiphilus, Sutterella wadsworthensis, and Faecalibacterium prausnitzii. Notably, F. prausnitzii, an organism often associated with butyrate production and anti-inflammatory commensal activity, was found elevated rather than depleted in these UC patients.

What are the greatest implications of this study?

The findings suggest that ulcerative colitis in this Russian cohort is associated with distinct shifts in gut microbial genera and species relative to healthy controls, expanding the geographic evidence base for microbiota-UC associations. The unexpected increase in Faecalibacterium and F. prausnitzii, rather than the depletion sometimes reported elsewhere, highlights that microbial signatures in UC may vary by population and underscores the need for region-specific microbiome characterization. These results support continued investigation into the intestinal microbiota as a factor in UC pathogenesis rather than establishing a definitive causal mechanism.

What was studied?

The gut microbiota can affect human metabolism, immunity, and other biologic pathways through the complex gut-kidney axis (GKA), and in turn participate in the occurrence and development of kidney disease. In this study, 39 patients with stage 4-5 chronic kidney disease (CKD) and 40 healthy individuals were recruited and 16S rDNA sequencing was performed to analyze the V3-V4 conserved regions of their microbiota. A total of 795 operational taxonomic units (OTUs) shared between groups or specific to each group were obtained, among which 255 OTUs with significant differences between the two groups were identified (P<0.05). Adonis differential analysis showed that the diversity of gut microbiota was highly correlated with CKD stages 4-5. Additionally, 61 genera with differences in the two groups were identified (P<0.05) and 111 species with significant differences in the phyla, classes, orders, families, and genera between the two groups were identified (P<0.05). The differential bacterial genera with the greatest contribution were, in descending order: c_Bacteroidia, o_Bacteroidales, p_Bacteroidetes, c_Clostridia, o_Clostridiales, etc. Those with the greatest contribution in stages 4-5 CKD were, in descending order: p_Proteobacteria, f_Enterobacteriaceae, o_Enterobacteriales, c_Gammaproteobacteria, c_Bacilli, etc. The results suggest that the diversity of the microbiota may affect the occurrence, development, and outcome of the terminal stages of CKD.

What was studied?

This study examined whole metagenome sequences of cecum microbiomes from Ethiopian indigenous chickens raised at two different altitudes. Researchers compared microbial community composition, functional gene pathways, and antibiotic resistance gene abundance between the two locations. Functional profiling used the KEGG, eggNOG, and CAZy databases, and taxonomic differences were identified using LEfSe.

Who was studied?

The subjects were Ethiopian indigenous chickens sampled from two distinct geographical zones: the Afar district (Dulecha, 730 meters above sea level) and the Amhara district (Menz Gera Midir, 3300 meters above sea level). The abstract does not give an exact number of birds sampled, so the cohort is best described as cecum microbiome samples drawn from these two altitude-defined chicken populations.

What were the most important findings?

Cecum microbial populations in both groups were mainly dominated by Bacteroidetes and Firmicutes, and the two groups shared 2210 common genes. Coprobacter, Geobacter, Cronobacter, Alloprevotella, and Dysgonomonas were more abundant in the low-altitude Afar chickens than in the high-altitude Amhara chickens. Functional pathway analysis showed enrichment in metabolism, genetic information processing, environmental information processing, and cellular process categories, and this functional abundance was linked to nutrient absorption and microbial localization. Antibiotic resistance genes for LSM, cephalosporin, and tetracycline were significantly more abundant in the Afar (low-altitude) group than in the Amhara (high-altitude) group.

What are the greatest implications of this study?

The findings suggest that altitude and geographic location are associated with meaningful shifts in gut microbial composition, function, and antibiotic resistance gene burden in indigenous chickens. The higher abundance of resistance genes at lower altitude raises questions about environmental or management factors that could influence antibiotic resistance in poultry gut microbiomes. These results provide a baseline for understanding how environment shapes microbiome-linked traits relevant to poultry health and food safety in indigenous chicken populations.

What was studied?

Both maternal microbiota and helminth infection may alter offspring immunity but the relationship between these is underexplored. We hypothesized that maternal helminth exposure prior to pregnancy has lasting consequences on offspring intestinal microbiota and consequent immunity. Female BALB/c adult mice were infected with 500L3 Nippostrongylus brasiliensis (N brasiliensis). Infection was cleared by ivermectin treatment, and mice were mated 3 weeks post-infection (NbM). Control mice were not infected but were exposed to ivermectin (NvM). We analysed maternal gut microbiota during pregnancy, breastmilk microbiota and offspring faecal microbiota and immunity 2 weeks after delivery. During pregnancy, NbM (Mothers previously infected with Nippostrongylus brasiliensis) displayed significantly altered stool bacterial communities (R2  = .242; P = .001), with increased abundance of Enterococcaceae versus NvM (Naive mothers). Similarly, we observed a profound impact on breastmilk microbiota in NbM vs NvM. Moreover, NbM pups showed significantly altered gut microbial communities at 14 days of age versus those born to NvM with increased relative abundance of Coriobacteriaceae and Micrococcaceae. These changes were associated with alterations in pup immunity including increased frequencies and numbers of activated CD4 T cells (CD4 + CD44hi) in NbM offspring spleens. Taken together, we show that preconception helminth infections impact offspring immunity possibly through alteration of maternal and offspring microbiota.

What was studied?

This study characterized alterations in the gut microbiome associated with chronic kidney disease (CKD). The researchers analyzed fecal samples to compare microbial diversity, community composition, and predicted microbial functions between CKD patients and healthy controls. They also constructed and validated diagnostic classifiers for CKD based on microbial markers using a random forest model, and examined relationships between specific taxa, disease progression, and clinical indicators.

Who was studied?

A total of 520 fecal samples were collected from different regions of China. The discovery and comparison cohort included 110 patients with CKD and 210 healthy controls (HC). The classifier was further tested in a validation cohort of 49 CKD cases versus 63 HC, and in an extra diagnosis cohort from Hangzhou.

What were the most important findings?

Gut microbial diversity was significantly decreased in CKD patients compared with healthy controls, and the overall microbial community composition was distinctly different between groups. The genera Klebsiella and Enterobacteriaceae were enriched in CKD, while Blautia and Roseburia were reduced. Fifty predicted microbial functions, including tryptophan and phenylalanine metabolism, increased in CKD, while 36 functions, including arginine and proline metabolism, decreased. A five-marker microbial classifier achieved an area under the curve (AUC) of 0.9887 in the discovery cohort, 0.9512 in the validation cohort, and 0.8986 in the extra Hangzhou diagnosis cohort, and Thalassospira and Akkermansia increased with CKD progression.

What are the greatest implications of this study?

These findings indicate that CKD is associated with a distinct, less diverse gut microbial community and altered amino acid metabolism pathways. The high diagnostic accuracy of the identified microbial markers across discovery, validation, and independent cohorts suggests gut microbiome signatures could serve as a non-invasive tool for CKD detection. The correlation between specific taxa and clinical indicators, along with taxa that shift with disease progression, points to the gut microbiome as a potential avenue for monitoring CKD severity.

What was studied?

Lung cancer (LC) is one of the most serious malignant tumors, which has the fastest growing morbidity and mortality worldwide. A role of the lung microbiota in LC pathogenesis has been analyzed, but a comparable role of the gut microbiota has not yet been investigated. In this study, the gut microbiota of 30 LC patients and 30 healthy controls were examined via next-generation sequencing of 16S rRNA and analyzed for diversity and biomarkers. We found that there was no decrease in significant microbial diversity (alpha diversity) in LC patients compared to controls (P observed = 0.1422), while the composition (beta diversity) differed significantly between patients and controls (phylum [stress = 0.153], class [stress = 0.16], order [stress = 0.146], family [stress = 0.153]). Controls had a higher abundance of the bacterial phylum Actinobacteria and genus Bifidobacterium, while patients with LC showed elevated levels of Enterococcus. These bacteria were found as possible biomarkers for LC. A decline of normal function of the gut microbiome in LC patients was also observed. These results provide the basic guidance for a systematic, multilayered assessment of the role of the gut microbiome in LC, which has a promising potential for early prevention and targeted intervention.

What was studied?

Condyloma acuminatum (CA) is a benign epithelium hyperplasia mainly caused by human papillomavirus (HPV), which is now the second most common viral sexually transmitted infection (STI) in China. In total, 90% of CA patients are caused by the low-risk HPV 6 and 11. Aside from low-risk HPV infection there are likely other factors within the local microenvironment that contribute to CA and there has been related research before. In this study, 62 vaginal specimens were analyzed using 16S rRNA gene sequencing. The diversity of the vaginal microbiota was higher and the composition was different with LR-HPV infection. While the relative abundance of dominant Firmicutes was lower, Actinobacteria, Proteobacteria, and Fusobacteria phyla were significantly higher; at the genus level Gardnerella, Bifidobacterium, Sneathia, Hydrogenophilus, Burkholderia, and Atopobium were higher. This study firstly confirmed a more accurate and comprehensive understanding of the relationship between low-risk HPV infection and vaginal microbiota, in order to provide a theoretical basis for further research on the occurrence and development of CA.

What was studied?

The aim of this study was to investigate the characteristics and composition of intestinal microbiota in children with refractory epilepsy after ketogenic diet (KD) therapy and to explore the bacterial biomarkers related to clinical efficacy.

Who was studied?

We prospectively analyzed 20 patients (14 males, 6 females) treated with KD. Clinical efficacy, electroencephalogram (EEG) changes, and laboratory tests were evaluated, and fecal specimens were obtained prior to and 6 months after therapy. The composition of gut microbiota was analyzed by 16S rDNA sequencing, and we screened the possible flora associated with efficacy of the KD.

What were the most important findings?

After 6 months of treatment, 2 patients were seizure free, 3 had ≥ 90% seizure reduction, 5 had a reduction of 50-89%, and 10 had < 50% reduction. All 10 responders showed an improvement in EEG. Compared with baseline, fecal microbial profiles showed lower alpha diversity after KD therapy and revealed significantly decreased abundance of Firmicutes and increased levels of Bacteroidetes. We also observed that Clostridiales, Ruminococcaceae, Rikenellaceae, Lachnospiraceae, and Alistipes were enriched in the non-responsive group.

What are the greatest implications of this study?

The results show that the KD can reduce the species richness and diversity of intestinal microbiota. The changes of gut microbiota may be associated with different efficacy after KD, and specific gut microbiota may serve as an efficacy biomarker and a potential therapeutic target in patients with refractory epilepsy.

What was studied?

This study examined the gut and oral microbiome in Behcet's disease (BD), a recurring inflammatory disease that can cause irreversible blindness. Researchers used metagenomic sequencing of fecal samples and 16S rRNA gene sequencing of saliva samples to compare microbial composition and biological function between BD patients and healthy controls. They then transplanted pooled fecal samples from active BD patients into mice undergoing experimental autoimmune uveitis (EAU) to test whether the gut microbiome could causally influence disease development.

Who was studied?

The human cohort consisted of 32 patients with active Behcet's disease and 74 healthy controls, who each provided fecal and saliva samples. The animal component of the study used B10RIII mice with induced experimental autoimmune uveitis, a model used to study the eye inflammation seen in BD. Together these groups allowed comparison of microbial signatures in humans alongside a causal test in an animal model.

What were the most important findings?

Fecal samples from active BD patients were enriched in Bilophila species, a sulfate-reducing bacteria (SRB), along with several opportunistic pathogens including Parabacteroides and Paraprevotella species. This enrichment occurred alongside a lower level of butyrate-producing bacteria compared to healthy controls. These shifts point to a gut microbial imbalance involving sulfate-reducing organisms and reduced beneficial short-chain fatty acid producers in BD patients.

What are the greatest implications of this study?

The findings suggest that gut microbiome composition, particularly the expansion of sulfate-reducing bacteria like Bilophila and the loss of butyrate producers, may contribute to the inflammatory processes underlying Behcet's disease. Using fecal transplantation into an autoimmune uveitis mouse model supports the idea that the gut microbiome may play a causal role rather than simply reflecting disease state. This work highlights the gut microbiome, and specifically sulfate-reducing and butyrate-producing bacteria, as a potential target for understanding or managing BD-related inflammation.

What was studied?

This study examined how conventional anti-tuberculosis drug therapy affects the intestinal microbiome. Researchers used 16S rRNA sequencing to longitudinally track microbial diversity and community composition in Mycobacterium tuberculosis-infected mice treated with the standard isoniazid-rifampin-pyrazinamide (HRZ) regimen. They also tested each antibiotic individually and in various combinations to identify which drug or drugs drove any observed changes.

Who was studied?

The study population was Mtb-infected mice, not human subjects. The abstract does not give an exact number of animals, but it describes longitudinal sampling across the treatment course and a post-treatment follow-up period of at least three months. Comparisons were made across mice receiving monotherapy, different combination therapies, and the full HRZ regimen.

What were the most important findings?

HRZ treatment caused only a transient dip in microbial diversity, but it triggered an immediate, marked, and reproducible shift in gut community structure that persisted throughout therapy and for at least three months after stopping treatment. Members of the order Clostridiales decreased in relative frequency during treatment, while the family Porphyromonadaceae increased afterward. Experiments isolating individual drugs identified rifampin as the major driver of these compositional alterations.

What are the greatest implications of this study?

Because this multi-drug regimen is administered to millions of people annually worldwide, a persistent, rifampin-driven dysbiosis lasting months beyond treatment could have broad public health relevance. The findings suggest that standard TB therapy leaves a durable signature on the gut microbiota rather than a transient one. This raises the question of whether such prolonged dysbiosis contributes to downstream health effects in treated patients, warranting further investigation in humans.