Given the ability to accurately map the microbial species and relative population sizes of the gut microbiome via 16S rRNA sequencing, researchers are generating an enormous amount of data linking specific characteristics of the gut microbiome to specific medical conditions, including the changes that take place with age. Here, researchers use data from patients with fibrosis in the lungs to mount an argument for Bifidobacterium adolescentis to be a beneficial species, and then test this proposal in aged mice. Increasing the presence of Bifidobacterium adolescentis in the gut microbiome of mice proves capable of attenuating fibrosis in the lung, making it a potentially interesting intervention. At present many forms of lung fibrosis are hard to treat and largely irreversible.
The global burden of pulmonary fibrosis is increasing. Recent studies have shown that some pulmonary fibrotic lesions caused by COVID-19 infection may persist for a long time. Emerging evidence suggested a critical association between gut microbiota and pulmonary fibrosis. In this study, the clinical follow-up data from post-COVID-19 patients indicated that those with higher CT image scores were older, had a significantly lower Blautia and Bifidobacterium to Streptococcus ratio (B/S index).
We examined whether Bifidobacterium adolescentis could attenuate bleomycin-induced pulmonary fibrosis in mice, with particular attention in the aging mice. Aging mice exhibited more severe pulmonary fibrosis after bleomycin induction, while the intervention of B. adolescentis attenuated the degree of pulmonary fibrosis in aging mice to a state similar to that of young mice. B. adolescentis alleviated inflammatory responses by enhancing the gut barrier, and reduced fibrotic marker expression (TGF-β, IL-17, α-SMA, Collagen I, Collagen III) by modulating PPAR and Th17 signaling pathways. Furthermore, B. adolescentis stabilized gut microbiota and increased the abundance of Bifidobacterium, Turicibacter, and norank_f_Desulfovibrionaceae, thereby suppressed the prostaglandin E2 (PGE2) and affected collagen deposition.
In conclusion, B. adolescentis alleviates pulmonary fibrosis through the gut-lung axis by regulating PGE2/PPAR/Th17 signaling, providing a promising therapeutic approach for pulmonary fibrosis management.
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