Lactobacillus paracasei L9 administration reshapes the gut microbiota to increase short-chain fatty acid production, which suppresses pulmonary Th17 cells and IL-17A through gut-lung axis signaling, thereby reducing collagen deposition and age-related pulmonary fibrosis in mice by 61%. This demonstrates a mechanistic pathway linking oral bacterial administration to lung tissue remodeling through immune cell migration regulation.
Key Points
- L9 increases SCFA-producing bacteria; serum propionic and butyric acid rise 97–193%
- SCFAs inhibit Th17 differentiation; pulmonary IL-17A and collagen synthesis decrease
- Gut-lung axis regulates immune migration; HSP47 expression drops 61%
Longevity Analysis
Age-related pulmonary fibrosis represents a progressive loss of lung function with few effective interventions. This research establishes that oral microbial administration can reverse fibrotic pathology through a cross-system immune regulatory mechanism. The pathway illuminates how the metabolic output of commensal bacteria—specifically short-chain fatty acids—reaches systemic circulation and reshapes immune cell behavior in distant tissues. This expands the therapeutic window for fibrotic disease from direct pharmacological intervention to upstream manipulation of microbial metabolism and immune tolerance, offering a precision nutrition strategy that works within the body's own regulatory architecture rather than against pathological endpoints.
Original published by Wiley Aging Cell, by Ran Bi, Yiran Zhang, Wen Zhang, Chenhong Shi, Ziyu Qiao, Rui Quan, Yanan Sun, Juan Chen, Ran Wang, Fazheng Ren, Yixuan Li .