Divine Aleru, Microbiome Signatures Research Coordinator

Enterococcus faecium (VREfm) has become a major healthcare threat due to its ability to acquire resistance and adapt to both clinical and environmental conditions. This review calls for new strategies to combat VREfm, emphasizing its transmission through multiple routes and the need for better diagnostic and treatment approaches.

Enterococcus faecalis utilizes five distinct iron uptake systems, including novel transporters, to maintain iron homeostasis and support virulence. Heme acquisition also plays a critical role in its pathogenesis. Targeting these transporters offers a promising approach for treating E. faecalis infections.

What was studied?This study examined the role of manganese (Mn) acquisition in the virulence of Enterococcus faecalis. Researchers identified and characterized the key manganese transport systems in E. faecalis, focusing on the ABC-type transporter EfaCBA and two Nramp-type transporters, MntH1 and MntH2. They tested how these transport systems contribute to bacterial growth in manganese-limited environments […]

What was studied?This study examined the Fsr quorum-sensing system in Enterococcus faecalis and its role in regulating the surface display of the collagen-binding protein Ace, a key virulence factor. Researchers investigated how disruption of the Fsr system, as well as GelE protease activity, influenced the expression of Ace on the cell surface, its ability to […]

Enterococcus faecium adapts through gene transfer and resistance mechanisms, making it a major cause of hospital infections. The study emphasizes the importance of genomic surveillance and the development of novel therapeutics like phage therapy and microbiota-based treatments to control the spread of VREfm infections.

VanB Enterococcus strains show inducible vancomycin resistance, enabling microbiome persistence and infection risk. Diagnostic methods reliably detect resistant strains, but low-level resistance may be missed. Enterococcus resistance expansion represents a key microbiome signature associated with hospital infection and treatment failure.

What was reviewed?This review examined how Enterococcus faecalis and Enterococcus faecium regulate VanA- and VanB-type glycopeptide resistance, which enables survival during vancomycin and related antibiotic exposure. The authors reviewed molecular, genetic, and microbiological evidence explaining how resistance genes alter peptidoglycan synthesis and how regulatory systems activate resistance in response to antibiotic exposure. The review focused […]

What was reviewed?This review examined how Enterococcus faecalis and Enterococcus faecium adapt to the gut microbiome, hospital environments, and host tissues through genetic plasticity, antimicrobial resistance, and virulence factor acquisition. The authors reviewed microbiological, genomic, and clinical evidence explaining how Enterococcus survives environmental stress, acquires resistance genes, and transitions from a gut microbiome commensal into […]

Enterococcus develops antibiotic resistance through genetic adaptation, enabling microbiome dominance and infection persistence. Resistance mechanisms allow Enterococcus to survive antibiotic exposure, expand in the gut microbiome, and spread resistance genes, making Enterococcus expansion a key microbiome signature linked to infection risk and antimicrobial resistance.

Enterococcus faecalis uses pheromone signaling to detect microbiome conditions, transfer antibiotic resistance genes, and activate virulence. This system promotes microbiome persistence, bacterial aggregation, and infection risk, making pheromone signaling an important microbiome signature of Enterococcus pathogenicity.

Enterococcus faecalis pili and adhesins enable microbiome persistence, collagen adherence, biofilm formation, and urinary tract infection. Loss of these factors reduces microbiome colonization and infection severity, identifying pili and adhesins as key microbiome virulence signatures linked to infection risk.

This review shows that Enterococcus expands during microbiome disruption, forms polymicrobial biofilms, and activates virulence factors that promote colonization, immune evasion, and systemic infection, identifying Enterococcus as a microbiome-driven pathobiont linked to increased infection risk and poor clinical outcomes.

Cytolysin allows Enterococcus faecalis to disrupt the microbiome, kill competitors, evade immune defenses, and increase infection severity. This toxin promotes microbial imbalance, pathogen expansion, and systemic infection, making cytolysin a key microbiome virulence factor and clinical biomarker.

Enterococcus faecalis regulates immune tolerance and microbiome stability but becomes pathogenic during dysbiosis. It increases IgA production, modulates inflammatory signaling, and strengthens gut barrier function in eubiosis. In dysbiosis, it expands, evades immune clearance, promotes inflammation, and contributes to systemic infections, making it a key microbiome biomarker of immune and microbial imbalance.

Enterococcus faecalis is a gut‑adapted, Gram‑positive, non‑spore‑forming facultative anaerobe that becomes an important opportunistic pathogen in healthcare when host barriers are breached or antibiotics select for enterococcal overgrowth. Its clinical impact is driven more by persistence, adhesion, and biofilm biology, quorum‑regulated secreted effectors (fsr‑controlled gelatinase GelE), and high genome plasticity than by a broad repertoire of classical tissue‑destroying toxins. Antimicrobial decision‑making must account for the intrinsic poor activity of cephalosporins, the potential for transferable glycopeptide resistance mediated by van gene clusters, and the need for regimen selection in endocarditis that respects synergy/tolerance and local high‑level aminoglycoside resistance patterns. 

This study showed that vaccination against Clostridium perfringens type C protects piglets by generating neutralizing antibodies against beta toxin, preventing microbiome-driven intestinal necrosis and infection risk. Passive immunity depends on sufficient maternal antibody production and transfer through colostrum, which can be improved through optimized vaccination protocols.

This review expands the Clostridium perfringens toxinotyping scheme to include toxinotypes F and G, linking enterotoxin and NetB production to specific microbiome-driven diseases. It highlights plasmid-mediated toxin transfer, improved microbial classification, and enhanced diagnostic precision for microbiome-associated enteric and systemic infections.

What was reviewed?This review examined the biological mechanisms, clinical applications, and translational potential of hyperbaric oxygen therapy (HBOT), a treatment that delivers 100% oxygen under elevated atmospheric pressure to increase oxygen availability in tissues. The authors analyzed how HBOT improves oxygen diffusion, enhances angiogenesis, regulates immune responses, and exerts antimicrobial effects, and they evaluated its […]

This review showed that toxin-producing Clostridium perfringens drives necrotizing infections by disrupting microbiome balance, destroying tissue, and promoting rapid pathogen expansion and disease progression.

This review showed that toxin plasmids control virulence in Clostridium perfringens by enabling toxin gene transfer between microbiome strains, allowing commensal bacteria to become pathogenic and increasing infection risk.

This study showed that Clostridium perfringens spore germination depends on specific germinant receptors, especially GerK, which detect nutrients like potassium and amino acids. GerK controls dipicolinic acid release, metabolic activation, and colony formation, establishing a direct link between environmental nutrient sensing and pathogen activation within the microbiome.

This review explains how the VirS/VirR regulatory system controls toxin production and virulence in Clostridium perfringens. Microbiome signals activate toxin genes, enabling the bacterium to transition from commensal colonizer to pathogenic organism and cause tissue damage, infection, and disease.

This review explains how Clostridium perfringens enterotoxin causes gastrointestinal disease by binding claudins and forming pores in intestinal epithelial cells. Toxin production during sporulation disrupts gut barrier integrity, promotes diarrhea, and contributes to microbiome-associated disease, especially following antibiotic exposure or microbial imbalance.

This study shows that toxin-neutralizing antibodies protect against Clostridium perfringens intestinal damage by blocking alpha toxin and perfringolysin O. These toxins drive microbiome-associated tissue necrosis, and antibody neutralization prevents cell death and infection progression.

This review explains how Clostridium perfringens toxins disrupt microbiome-host interactions by damaging cell membranes, forming pores, and activating intracellular pathways that cause cell death, inflammation, and disease. These toxin-driven mechanisms represent key microbiome signatures associated with infection severity and pathogenic progression.

This study shows that microbiome nutrients such as arginine, zinc, and vitamins regulate alpha-toxin production in Clostridium perfringens. Toxin production depends on specific nutrient conditions rather than bacterial growth alone, establishing microbiome nutrient balance as a key determinant of virulence and infection risk.

This study shows that FeoB iron transport controls Clostridium perfringens growth, toxin production, and microbiome survival. Iron acquisition regulates virulence, metabolism, and infection risk, making FeoB a key microbiome signature linked to pathogenic fitness and disease severity.

This study shows that zinc stabilizes Clostridium perfringens alpha-toxin and protects it from protease degradation, while calcium promotes protease production that destroys toxin. These microbiome metal ion interactions regulate toxin activity, virulence, and infection risk.

This review explains how Clostridium perfringens uses sporulation to survive microbiome stress, resist antibiotics, and transmit infection between hosts. Sporulation enables toxin production, microbiome persistence, and disease progression. Spores resist environmental and immune defenses, allowing long-term survival and increasing risk of infection recurrence and transmission.

This review shows how Clostridium perfringens sporulation enables toxin production, microbiome persistence, and intestinal disease.

This review explains how Clostridium spores enable microbiome survival, toxin production, and infection through sporulation and germination.

This guideline explains how microbiome-derived pathogens cause skin and soft tissue infections and highlights key microbial signatures linked to severe disease.

This study shows how the pCW3 plasmid enables transfer of tetracycline resistance and toxin genes in Clostridium perfringens, identifying key microbiome mechanisms driving resistance and virulence spread.

This review explains how mobile plasmids drive antibiotic resistance and toxin spread in Clostridium perfringens, identifying key microbiome mechanisms behind treatment resistance and pathogenicity.

This review explains how Clostridium perfringens epsilon toxin activates in the gut microbiome and causes brain injury, vascular damage, and systemic disease.

This study defines how the NetB toxin from Clostridium perfringens forms membrane pores and drives enteric disease, linking toxin structure to microbiome-associated virulence and epithelial damage.

This review explains how Clostridium perfringens type F causes gastrointestinal disease through microbiome colonization, sporulation, and enterotoxin production. The toxin disrupts intestinal epithelial barriers, enabling infection, inflammation, and diarrhea, highlighting toxin detection and microbiome stability as key factors in preventing foodborne and antibiotic-associated gastrointestinal disease.

This review explains how Clostridium perfringens causes necrotic disease through microbiome disruption, toxin production, and immune suppression. Microbiome imbalance increases pathogen abundance, while microbial metabolites can reduce virulence, highlighting microbiome stability as a key protective factor and therapeutic target in necrotic enteritis and systemic infection.

This review explains how Clostridium perfringens uses toxin production, plasmid gene transfer, and microbiome colonization to cause intestinal and systemic disease. Virulence regulation, sporulation, and quorum sensing allow rapid pathogenic expansion, highlighting microbiome disruption and toxin gene detection as key clinical risk factors.

This genome sequencing study revealed how Clostridium perfringens survives in the gut microbiome and causes disease. Virulence genes, toxin regulation, and host-dependent metabolism enable tissue destruction and rapid growth, highlighting microbiome-driven pathogenicity and identifying genetic targets for improved diagnostics and therapeutic interventions.

This genomic study identified a Clostridium perfringens strain carrying both enterotoxin and NetB toxin genes, revealing microbiome-driven virulence evolution through plasmid transfer. The findings highlight microbiome gene exchange as a key driver of pathogenicity and emphasize the need for genomic surveillance to detect emerging toxin-producing strains.

This genomic study of 372 Clostridium perfringens strains revealed extreme genetic diversity, widespread toxin genes, and high antimicrobial resistance. Microbiome-associated virulence factors enable host colonization, intestinal disease, and zoonotic transmission, highlighting the importance of microbiome surveillance and genomic diagnostics to prevent foodborne illness and antibiotic-resistant infections.

This review explains how NetB toxin enables Clostridium perfringens to shift from a gut microbiome commensal to a toxin-producing pathogen. NetB disrupts intestinal epithelial barriers, promotes bacterial dominance, and drives necrotic enteritis, highlighting toxin detection and microbiome stability as key targets for disease prevention.

This review explains how Clostridium perfringens shifts from a gut microbiome commensal to a toxin-producing pathogen. Genomic diversity, toxin genes, antibiotic resistance, and microbiome disruption drive gastrointestinal disease, including food poisoning and necrotizing enterocolitis, highlighting its importance as a microbiome biomarker and therapeutic target.

This review explains how Clostridium perfringens functions as a gut microbiome commensal and toxin-producing pathogen. Toxin genes, plasmid virulence, antimicrobial resistance, and microbiome disruption drive gastrointestinal disease, antibiotic-associated diarrhea, and food poisoning, highlighting the importance of toxin detection and microbiome stability in clinical management.

Clostridium perfringens is a fast-growing, Gram-positive, spore-forming anaerobe and a major toxin-mediated pathogen affecting humans and animals. Widely distributed in soil, food, and gastrointestinal microbiota, it causes diseases ranging from food poisoning and antibiotic-associated diarrhoea to life-threatening clostridial myonecrosis. Its pathogenicity is driven by diverse plasmid-encoded toxins, including α-toxin, enterotoxin, and perfringolysin O, while conjugative mobile genetic elements facilitate rapid dissemination of antimicrobial resistance and virulence traits. Genome-informed toxinotyping and molecular surveillance are therefore essential for accurate risk assessment, clinical management, and outbreak control.

This study reveals that Fusobacterium animalis is linked to increased immune gene expression and microsatellite instability in CRC. It suggests Fusobacterium’s role in tumor progression, offering insights into potential biomarkers and therapeutic strategies for CRC patients.

This study uncovers the dual role of HmuF and FldH in Fusobacterium nucleatum’s anaerobic heme degradation, highlighting their functions in heme trafficking and reduction of anaerobilin, with implications for targeted therapeutic strategies.

What was studied?This study explored the role of Fusobacterium nucleatum’s outer membrane proteins, Fap2 and RadD, in inducing cell death in human lymphocytes. It focused on how these proteins, identified as part of the type Va autotransporter family, contribute to the bacterium’s virulence. The study examined the mechanisms by which Fap2 and RadD trigger cell […]

This study reveals Fn-Dps, a virulence factor from Fusobacterium nucleatum, as a key player in colorectal cancer metastasis, immune evasion, and erythrocyte disruption, highlighting its potential as a target for therapeutic intervention and a biomarker for CRC.

This review explores the role of Fusobacterium nucleatum in colorectal cancer, its impact on tumor progression, metastasis, immune modulation, and chemoresistance, and proposes potential strategies for CRC prevention and treatment.

This study identifies Fusobacterium nucleatum W1481 as a potential new subspecies, with unique genomic islands and antibiotic resistance mechanisms, highlighting its role in periodontal disease and potential for further clinical research.

This study explores how Fusobacterium nucleatum promotes chemoresistance in colorectal cancer by activating autophagy and altering microRNA expression, highlighting potential therapeutic avenues.

This study identifies Fusobacterium nucleatum as a significant pathogen in primary endodontic infections, strongly associated with clinical features like pain and swelling. The higher detection rate by PCR emphasizes the need for targeted treatments to eliminate this bacterium and improve endodontic outcomes.

What was studied?This study investigated the impact of Fusobacterium nucleatum’s FadA antigen on the competing endogenous RNA (ceRNA) network involving ANXA2 (Annexin A2) and its role in the progression of colorectal cancer (CRC) and adenomatous polyps (AP). Specifically, it examined how the FadA antigen contributes to the upregulation of ANXA2 through interactions with LINC00460 and […]

This study shows that Fusobacterium nucleatum-derived extracellular vesicles activate the AIM2 inflammasome in intestinal epithelial cells, leading to pyroptosis and exacerbating ulcerative colitis. Targeting this pathway may offer a promising therapeutic strategy to alleviate UC progression.

This study explores how Fusobacterium nucleatum contributes to chemoresistance in colorectal cancer by activating the autophagy pathway through the downregulation of specific microRNAs, offering potential targets for improving chemotherapy outcomes.

This study identifies MegL as the major enzyme for H2S production in Fusobacterium nucleatum, crucial for bacterial fitness, antibiotic resistance, and virulence in preterm birth, offering potential therapeutic targets to manage F. nucleatum infections.

This study reveals a significant increase in penicillin-resistant Fusobacterium nucleatum in children due to beta-lactamase production, highlighting the role of antimicrobial exposure in the rise of resistance and the need for alternative treatment strategies in pediatric infections.

What was studied?This study investigated the production of beta-lactamase and antimicrobial susceptibility profiles of Fusobacterium nucleatum isolates from the oral microbiota of young children. The research aimed to identify the frequency of beta-lactamase production among different F. nucleatum subspecies, assess the associated resistance to antibiotics, and evaluate potential alternative treatments for infections caused by this […]

This review discusses how Fusobacterium nucleatum adhesin RadD binds to CD147, promoting colorectal cancer proliferation. Targeting RadD may provide new therapeutic strategies for CRC treatment.

This study reveals that Fusobacterium nucleatum FadA promotes CRC through binding E-cadherin, activating beta-catenin signaling and inflammation. These findings suggest new diagnostic and therapeutic strategies targeting FadA to reduce CRC progression.

This study identifies the role of Fusobacterium nucleatum Fap2 in mediating bacterial enrichment in colorectal cancer by binding to tumor-expressed Gal-GalNAc. Targeting this interaction could reduce Fusobacterium’s potentiation of CRC, offering new therapeutic and diagnostic opportunities.

This review explores Fusobacterium nucleatum’s role as a transboundary pathogen in diseases like colorectal cancer and inflammatory bowel disease, highlighting its virulence factors, immune modulation, and complex microbial interactions. It offers insights into potential therapeutic strategies targeting this pathogen and its microbial networks.

This review discusses Fusobacterium nucleatum’s pivotal role in diseases like colorectal cancer and inflammatory bowel disease, emphasizing its pathogenic mechanisms, including immune evasion and tumor progression, and exploring novel diagnostic and therapeutic approaches targeting this bacterium.

This study explores the prevalence of Fusobacterium nucleatum in primary and secondary endodontic infections, highlighting its association with clinical symptoms like pain and swelling. PCR detection showed higher prevalence, emphasizing the pathogen’s role and the need for focused endodontic treatments.

Fusobacterium nucleatum is a Gram-negative, anaerobic bacterium commonly found in the oral cavity, where it plays a crucial role in the formation of biofilms. Beyond its presence in the mouth, Fn is implicated in a variety of systemic conditions, including periodontal disease, colorectal cancer, and inflammatory bowel disease. Known for its ability to coaggregate with other bacteria, Fn’s pathogenic potential is magnified in dysbiotic microbial communities, making it a key player in polymicrobial infections. The bacterium utilizes multiple virulence factors such as FadA and Fap2, which facilitate adhesion to host tissues and immune evasion, ultimately contributing to its role in chronic and inflammatory diseases.

This review shows that dietary polyphenols selectively increase Akkermansia muciniphila, improving gut barrier function and metabolic outcomes through microbiome-mediated mechanisms rather than direct antioxidant effects.

This review positions Akkermansia muciniphila as a key regulator of oxidative stress through mucin metabolism, bioactive proteins, and gut–organ signaling. Its clinical impact spans metabolic, inflammatory, and neurodegenerative conditions, with benefits strongly dependent on strain and host context.

What was reviewed?This systematic review evaluated how bioactive compounds, including dietary fibers, polyphenols, antioxidants, human milk oligosaccharides, and selected pharmaceuticals, influence the abundance and functional activity of Akkermansia muciniphila in the gut. Following PRISMA 2020 guidelines, the authors synthesized experimental evidence from 2004 to 2025 to clarify mechanisms through which these compounds modulate A. muciniphila […]

This review summarizes evidence that diet, prebiotics, and drugs such as metformin can increase Akkermansia muciniphila, a mucus-associated bacterium linked to improved metabolic health and reduced inflammation.

This study shows that live Akkermansia muciniphila protects against diet-induced obesity by selectively remodeling intestinal mucus glycan composition and barrier gene expression, rather than altering overall microbiome structure.

This study shows how gut bacterial mucinases precisely cleave O-glycan-rich glycoproteins using specialized structural adaptations, enabling controlled mucus turnover while preserving barrier function and explaining how mucin-degrading microbes can be beneficial or harmful depending on context.

This study shows that Akkermansia muciniphila uses dietary polyphenols as iron carriers, enabling growth under iron limitation and outcompeting pathogenic bacteria through advanced iron acquisition systems.

This review highlights Akkermansia-derived extracellular vesicles as powerful regulators of gut barrier function, immune balance, metabolism, and cancer response, positioning them as promising cell-free microbiome therapeutics.

This study shows that Akkermansia muciniphila survives gastrointestinal stress through aggregation, adheres preferentially to mucus-secreting intestinal cells, and interacts with human mucins via specific proteins, supporting its therapeutic potential while highlighting dose-dependent safety considerations.

This review highlights Amuc_1100, a bioactive membrane protein from Akkermansia muciniphila, as a potent immunometabolic regulator that strengthens gut barrier function, reshapes microbiome composition, and modulates systemic inflammation across metabolic, inflammatory, and oncologic disease models.

This review explains how Akkermansia muciniphila proteins, not just the bacterium itself, regulate immunity, metabolism, gut barrier integrity, cancer response, and neuroinflammation, highlighting their emerging role as next-generation postbiotic therapeutics.

This review explains how mucin-degrading gut bacteria regulate barrier integrity, immunity, and disease risk in a context-dependent manner. It highlights why microbes such as Akkermansia muciniphila can be protective or harmful depending on diet, strain, and host immune status.

This study shows that Akkermansia muciniphila produces a uniquely structured lipooligosaccharide that preferentially activates anti-inflammatory TLR2 signaling while limiting TLR4-driven endotoxin responses. The findings explain how this Gram-negative symbiont supports immune balance and metabolic health.

This review explores when mucus degradation by Akkermansia muciniphila supports gut health and when it harms barrier integrity. Evidence shows its effects depend on host context, microbial balance, and mucus renewal capacity, reframing it as a condition-dependent microbiome signal rather than a universal probiotic.

This study shows that excessive Akkermansia muciniphila colonization damages the intestinal mucus barrier and tight junctions in colorectal cancer models, worsening inflammation and disease progression. Findings highlight its role as a context-dependent microbe rather than a universally beneficial probiotic.

This review summarizes evidence that Akkermansia muciniphila reduces inflammation and improves metabolic health by strengthening the gut barrier and regulating immune signaling. Findings support its role as a next-generation probiotic for obesity, diabetes, and related inflammatory conditions.

This review shows that Akkermansia muciniphila protects against bacterial and viral infections by strengthening gut barriers and regulating systemic immunity. Evidence supports its role as a next-generation probiotic with effects extending beyond metabolism into infection and immune resilience.

This study shows that antibiotics can select Akkermansia muciniphila variants that lose their ability to protect against obesity and metabolic dysfunction. The findings reveal a direct mechanistic link between antibiotic exposure, altered microbiome function, and chronic metabolic disease risk.

This study shows that human-derived Akkermansia muciniphila strains carry limited, mostly nonfunctional antibiotic resistance traits. Phenotypic testing confirms low risk of transferable resistance, supporting its safety as a next-generation probiotic and microbiome biomarker.

This review explains how Akkermansia muciniphila supports gut barrier integrity, immune balance, and metabolic health. Evidence highlights its role as a key microbiome signal across obesity, inflammation, and aging, with postbiotic strategies showing strong clinical promise.

This review synthesizes evidence showing Akkermansia muciniphila supports gut barrier integrity, immune balance, and metabolic health through mucin degradation, SCFA production, and bioactive proteins, with emerging human trials confirming safety and therapeutic promise.

What was reviewed?This review synthesized experimental, translational, and clinical evidence describing the biological functions of Akkermansia muciniphila in intestinal-related diseases. The authors evaluated how this mucin-degrading bacterium contributes to intestinal homeostasis, immune regulation, and metabolic balance, with emphasis on mechanistic pathways rather than descriptive abundance alone. The review integrated findings on live bacteria, pasteurized cells, […]

This review examines how Akkermansia muciniphila shapes gut immune signaling to reduce inflammation, obesity, and diabetes risk. Evidence shows that its abundance and derived proteins strengthen the intestinal barrier, suppress pro-inflammatory cytokines, and improve metabolic outcomes across experimental models and early human trials.

This review maps where Akkermansia muciniphila appears across the human gut and beyond, from early infancy to old age. Evidence links higher abundance with stronger mucus-barrier function and better metabolic health, while lower levels track with IBD, appendicitis severity, obesity, and dysglycemia.

Akkermansia muciniphila is a mucus-layer specialist that has shifted from “odd gut commensal” to one of the most mechanistically characterized next-generation probiotic candidates. First isolated from human feces using gastric mucin as the sole carbon and nitrogen source, it is adapted to life at the mucus–epithelium interface, where it converts host mucins into metabolites (notably acetate and propionate) that can feed other microbes and influence host physiology. Its genome encodes an unusually rich secretome for mucin foraging, dozens of predicted glycoside hydrolases, sulfatases, proteases, and sialidases, supporting stepwise dismantling of complex O-glycans and the mucin backbone.

This study explores the virulence mechanisms of Listeria monocytogenes, focusing on its surface proteins and iron acquisition systems, shedding light on potential therapeutic interventions and food safety strategies.

This study demonstrates that bacteriophage P100 is a safe and effective biocontrol agent for reducing Listeria monocytogenes in soft cheeses, offering a promising alternative to traditional antimicrobial agents.

This study demonstrates that the FOP bacteriophage cocktail effectively reduces Listeria monocytogenes levels in the gastrointestinal tract, without disturbing the gut microbiota, offering a promising alternative to antibiotics for treating or preventing Listeria infections.

This case report demonstrates the effectiveness of oral sulfamethoxazole in treating Listeria monocytogenes meningitis in a renal transplant patient, offering an alternative treatment approach for those allergic to penicillin.

This study explores copper resistance in Listeria monocytogenes, identifying how the csoR-copA-copZ operon, regulated by CsoR and CopZ, contributes to copper tolerance.

This study examines how Listeria monocytogenes uses two zinc uptake systems (ZurAM and ZinABC) to survive within the host, highlighting their importance for growth and virulence during infection.

This study explores the role of peroxidase enzymes in Listeria monocytogenes pathogenesis, revealing how the bacteria survive oxidative stress and how targeting specific enzymes could offer new therapeutic approaches for treating infections.

This study on Listeria monocytogenes reveals its mechanisms for acquiring iron from host proteins and external siderophores. Understanding these strategies aids in developing new treatments for infections.