Gut microbiota dysbiosis contributes to the development of chronic obstructive pulmonary disease

Background Dysbiosis of the gut microbiome is involved in the pathogenesis of various diseases, but the contribution of gut microbes to the progression of chronic obstructive pulmonary disease (COPD) is still poorly understood. Methods We carried out 16S rRNA gene sequencing and short-chain fatty acid analyses in stool samples from a cohort of 73 healthy controls, 67 patients with COPD of GOLD stages I and II severity, and 32 patients with COPD of GOLD stages III and IV severity. Fecal microbiota from the three groups were then inoculated into recipient mice for a total of 14 times in 28 days to induce pulmonary changes. Furthermore, fecal microbiota from the three groups were inoculated into mice exposed to smoke from biomass fuel to induce COPD-like changes. Results We observed that the gut microbiome of COPD patients varied from that of healthy controls and was characterized by a distinct overall microbial diversity and composition, a Prevotella-dominated gut enterotype and lower levels of short-chain fatty acids. After 28 days of fecal transplantation from COPD patients, recipient mice exhibited elevated lung inflammation. Moreover, when mice were under both fecal transplantation and biomass fuel smoke exposure for a total of 20 weeks, accelerated declines in lung function, severe emphysematous changes, airway remodeling and mucus hypersecretion were observed. Conclusion These data demonstrate that altered gut microbiota in COPD patients is associated with disease progression in mice model.

Automated summary

The gut microbiome of COPD patients differs from healthy controls, with distinct microbial diversity, Prevotella-dominated gut enterotype, and lower levels of short-chain fatty acids. Transplantation of fecal microbiota from COPD patients into mice led to elevated lung inflammation, while exposure to biomass fuel smoke exacerbated lung function decline, emphysematous changes, airway remodeling, and mucus hypersecretion in a COPD-like manner.