Gut microbiota dysbiosis has a causal effect on the severity of cigarette smoking (CS)–induced chronic obstructive pulmonary disease (COPD) pathogenesis, researchers reported in Gut.

Investigators established the gut microbiota–lung COPD axis with use of a murine CS model of chronic pulmonary inflammation, fecal microbiota transplantation (FMT), and antibiotics. Mice exposed to smoking for 12 weeks lost significant body weight and had increased infiltration of immune cells in bronchoalveolar lavage fluid. Histologic analysis of lung tissue sections showed that the CS-exposed mice had peripheral emphysematous changes, including alveolar wall destruction and enlargement of airspace, compared with control mice.

Treatment with antibiotics, as well as FMT, affected the composition of gut microbiota in the CS mice. Parabacteroides goldsteinii (Pg) was significantly, negatively associated with COPD severity.


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In addition, oral administration of isolated Pg MTS01 significantly ameliorated CS-induced COPD. This amelioration included reducing inflammation and improving cellular ribosomal biogenesis activity and mitochondrial functions in the intestines, systematically restoring aberrant amino acid metabolism in sera, and reducing lung tissue inflammation.

The lipopolysaccharide (LPS) that was derived from Pg-LPS acted as a toll-like receptor 4 antagonist and was an active component that ameliorated CS-induced COPD, noted the investigators.

“Our study highlighted the important causality role of gut microbiota in COPD pathogenesis and established the gut-lung COPD axis,” stated the researchers. “Pg MTS01 and Pg-LPS are potential therapeutic agents that may be developed into functional probiotics and postbiotics, respectively, to ameliorate COPD.”

Reference

Lai H-C, Lin T-L, Chen T-W, et al. Gut microbiota modulates COPD pathogenesis: role of anti-inflammatory Parabacteroides goldsteinii lipopolysaccharide. Gut. Published online March 9, 2021. doi: 10.1136/gutjnl-2020-322599