Home Research Feeds Gut microbiota composition can reflect immune responses of latent tuberculosis infection in patients with poorly controlled diabetes

Gut microbiota composition can reflect immune responses of latent tuberculosis infection in patients with poorly controlled diabetesOriginal paper

Researched by:

  • Karen PendergrassID

Last Updated: 2026-06-26

Karen Pendergrass
Karen Pendergrass

Karen Pendergrass is a microbiome researcher specializing in microbiome-targeted interventions (MBTIs). She systematically analyzes scientific literature to identify microbial patterns, develop hypotheses, and validate interventions. As the founder of the Microbiome Signatures Database, she bridges microbiome research with clinical practice. In 2012, based on her own investigative research, she became the first documented case of FMT for Celiac Disease, four years before the first published case study.

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Location
Taiwan
Sample Site
Feces
Species
Homo sapiens

What Was Studied?

This prospective observational study examined whether gut microbiota composition reflects host immune responses and latent tuberculosis infection (LTBI) status in patients with poorly controlled diabetes. Fecal microbiota were profiled by 16S rRNA gene sequencing of the V3-V4 hypervariable regions on the Illumina MiSeq platform, and LTBI was defined using the QuantiFERON-TB Gold In-Tube interferon-gamma release assay. Investigators compared taxonomic diversity and differential genera between LTBI and non-LTBI groups and built a random forest classifier from the most discriminating taxa.

Who Was Studied?

The cohort comprised 130 patients with poorly controlled diabetes (HbA1c greater than 9.0% within the prior year) recruited at Kaohsiung Medical University Hospital and National Taiwan University Hospital in Taiwan, of whom 43 had LTBI and 87 did not. Stool and blood samples were collected at enrollment. Patients who had used systemic antibiotics within three months prior to enrollment were excluded.

What Were the Key Findings?

Alpha-diversity did not differ between groups, but beta-diversity was significantly distinct (p=0.007 unweighted and p=0.002 weighted UniFrac). The LTBI group showed enrichment of Bacteroides (37.79% vs 29.72%, p=0.001) along with Alistipes and Blautia, and depletion of Prevotella_9 (2.53% vs 8.95%, p<0.001) together with Streptococcus and Actinomyces; LTBI patients also had lower serum IL-17F (p=0.025) and TNF-alpha (p=0.038). These taxa correlated with Th1/Th17 cytokine production, with Bacteroides inversely associated with IFN-gamma, IL-17A, IL-10, IL-22, and TNF-alpha, while Blautia showed positive correlations. A model using the six differential genera (Bacteroides, Streptococcus, Alistipes, Blautia, Prevotella_9, and Actinomyces) predicted LTBI status with an accuracy of 0.872 and an AUROC of 0.834.

What Are the Implications?

These findings suggest that the gut microbiota may modulate Th1/Th17-mediated immunity relevant to tuberculosis susceptibility in patients with poorly controlled diabetes, and that a microbiota-based signature could potentially aid LTBI detection in this high-risk population. Because the data are cross-sectional and associative, they cannot establish whether microbial shifts drive altered immune responses or merely accompany LTBI, and the predictive model requires external validation. The three-month antibiotic exclusion reduces but does not eliminate confounding from diet, glycemic control, and other host factors.

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