COPD肠道菌群作用机制：如何通过肺肠轴影响炎症与肺功能？

The core pathological mechanism of COPD is chronic inflammation in the lungs, and the gut microbiota can participate in inflammatory responses and influence the condition through direct or indirect means. On one hand, dysbiosis of the gut microbiota (reduced Gram-positive bacteria and increased Gram-negative bacteria) can damage the mucosal barrier, leading to translocation of pathogenic bacteria, which then migrate to the lungs via the circulatory system, causing inflammation. Additionally, dysbiosis of the microbiota, especially Gram-negative bacteria, and the disruption of the microbial community following antibiotic use can produce large amounts of endotoxins that enter the bloodstream and are transported to the lungs, causing endotoxin-induced lung injury and exacerbating COPD progression [47,49]. Some pathogenic bacteria (such as Enterobacteriaceae) can also activate the NF-κB pathway via the TLR4 signaling pathway, inducing inflammation and oxidative stress [51]. On the other hand, metabolic products of the gut microbiota, such as short-chain fatty acids (SCFAs), can reach the lungs via systemic circulation and, by activating GPR41 and GPR43 receptors or modulating the TLR1 signaling pathway, inhibit the production of pro-inflammatory factors, thereby reducing pulmonary and systemic inflammatory responses [50,51]. Furthermore, the degree of gut microbiota dysbiosis in stable COPD patients is positively correlated with inflammatory markers such as IL-6 and TNF-α, and negatively correlated with lung function indicators such as FEV1, suggesting that the gut microbiota can indirectly affect the condition by regulating inflammation and lung function [52].