Abstract
Although tuberculosis (TB) is a curable disease, it remains the foremost cause of death from a single pathogen. Globally, approximately 1.6 million people died of TB in 2017. Many predisposing factors related to host immunity, genetics and the environment have been linked to TB. However, recent evidence suggests a relationship between dysbiosis in the gut microbiome and TB disease development. The underlying mechanism(s) whereby dysbiosis in the gut microbiota may impact the different stages in TB disease progression, are, however, not fully explained. In the wake of recently emerging literature, the gut microbiome could represent a potential modifiable host factor to improve TB immunity and treatment response. Herein, we summarize early data detailing (1) possible association between gut microbiome dysbiosis and TB (2) the potential for the use of microbiota biosignatures to discriminate active TB disease from healthy individuals (3) the adverse effect of protracted anti-TB antibiotics treatment on gut microbiota balance, and possible link to increased susceptibility to Mycobacterium tuberculosis re-infection or TB recrudescence following successful cure. We also discuss immune pathways whereby the gut microbiome could impact TB disease and serve as target for clinical manipulation.
Highlights
Tuberculosis (TB) is an infectious disease caused by the non-motile, acid fast bacillus Mycobacterium tuberculosis (M.tb)
We summarize emerging data describing the association between the gut microbiome and lung immunity during TB disease
Reports investigating whether alterations in the gut microbiome contribute to bias in inter-individual levels of susceptibility to M.tb infection or response to TB drug treatment are still emerging
Summary
Tuberculosis (TB) is an infectious disease caused by the non-motile, acid fast bacillus Mycobacterium tuberculosis (M.tb). Antibiotic-induced changes in the gut diversity of M.tb-infected animals compromised mouse immunity and increased the ability of the pathogen to spread to other organs [38] This disruption in the gut microbiota was shown to modify the adaptive cell-mediated immune responses to M.tb, with Tregs expanding in numbers while IFN-γ and TNF-α- producing Th1 cells diminished in their frequencies. Depletion of Bifidobacterium and Lactobacillus with neomycin was associated with altered immune response to influenza A virus infection with concomitant increase in lung damage in a mouse model [55] This antibiotic-induced dysbiosis inhibited TLR7 signaling, the event of which reduced the secretion of the downstream pro-inflammatory cytokines IFN-γ and IL-17, with a simultaneous increase in the levels of IL-4 and IL-10.
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