Gut Microbiota Interactions in Pulmonary Tuberculosis

The gut microbiota exerts a profound influence on systemic immunity and plays a pivotal role in modulating susceptibility to and progression of pulmonary tuberculosis. A balanced microbial community maintains intestinal barrier integrity, regulates inflammatory mediators and fosters protective immune cell development. Perturbations induced by infection or antibiotic therapy can disrupt this equilibrium, leading to dysbiosis, increased gut permeability and altered signalling through the gut–lung axis. These changes may enhance Mycobacterium tuberculosis colonisation in the lung, impair anti-mycobacterial responses and contribute to variable treatment outcomes. Emerging research highlights the potential to harness microbial diagnostics, probiotics or microbiota-targeted interventions to improve prevention, detection and management of tuberculosis on a global scale.

Research from Nature Portfolio

A foundational study examined the long-term effects of standard anti-tuberculosis therapy on the human intestinal microbiome. Although overall diversity remained stable, multidrug regimens dramatically depleted key commensal taxa with immunomodulatory functions, and this altered community structure persisted for more than a year after treatment completion. The durable dysbiosis, characterised by loss of specific Clostridiales and other beneficial organisms, underscores the unintended ecological footprint of tuberculosis chemotherapy and suggests that recovery of gut microbial balance may be crucial for restoring robust host immunity and reducing the risk of reinfection.

Gut Microbiota Interactions in Pulmonary Tuberculosis publication trend

The graph below shows the total number of articles in gut microbiota interactions in pulmonary tuberculosis across all publications each year (not limited to Nature Index journals).

Technical terms

Dysbiosis: Imbalance in the composition or function of the microbial community leading to adverse host effects.

Gut–lung axis: Bidirectional communication network linking intestinal microbes and lung immunity through immune, neural and metabolic pathways.

Mendelian randomisation: Analytical method using genetic variants as proxies to infer causal relationships between exposures and outcomes.

Short-chain fatty acids: Metabolic by-products of microbial fermentation that regulate inflammation and barrier function.

Eubiosis: State of microbial homeostasis characterised by balanced diversity and functional resilience.

References

1. Longitudinal profiling reveals a persistent intestinal dysbiosis triggered by conventional anti-tuberculosis therapy. Microbiome (2017).
2. Intestinal microbiome dysbiosis increases Mycobacteria pulmonary colonization in mice by regulating the Nos2-associated pathways. eLife (2024).
3. Causal relationship between gut microbiota and tuberculosis: a bidirectional two-sample Mendelian randomization analysis. Respiratory Research (2024).
4. Gut microbiome, T cell subsets, and cytokine analysis identify differential biomarkers in tuberculosis. Frontiers in Immunology (2024).