AI Article Synopsis
- The study investigates the relationship between gut microbiota and lung health, particularly how obesity-induced gut dysbiosis may worsen tuberculosis infection and lung inflammation.
- Using a mouse model of high-fat diet-induced obesity and subsequent TB infection, the researchers found increased susceptibility and inflammation in obese mice.
- The findings emphasize the potential of modifying gut microbiota as a therapeutic strategy for improving responses to tuberculosis, especially in individuals with obesity-related complications.
Article Abstract
The microbiota of the gut-lung axis affects local and far-reaching immune responses and might also trigger chronic and inflammatory diseases. We hypothesized that gut dysbiosis induced by obesity, which coexists in countries with a high tuberculosis burden, aggravates the host susceptibility and the pulmonary damage tolerance. To assess our hypothesis, we used a model of high-fat diet (HFD)-induced obesity, followed by infection of C57BL/6 mice with . We showed that obesity increased the susceptibility, the pulmonary inflammation and IFN-γ levels in -infected mice. During the comorbidity obesity and tuberculosis, there is an increase of Bacteroidetes and Firmicutes in the lungs, and an increase of Firmicutes and butyrate in the feces. Depletion of gut microbiota by antibiotic treatment in the obese infected mice reduced the frequencies of CD4IFN-γIL-17 cells and IFN-γ levels in the lungs, associated with an increase of . Our findings reinforce the role of the gut-lung axis in chronic infections and suggest that the gut microbiota modulation may be a potential host-directed therapy as an adjuvant to treat TB in the context of IFN-γ-mediated immunopathology.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8303177 | PMC |
| http://dx.doi.org/10.3390/cells10071732 | DOI Listing |
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