RESUMO
Existing comprehensive management strategies for COPD effectively relieve the symptoms of patients, delay the deterioration of lung function, and prevent the progression of COPD through various means and multidisciplinary interventions. However, there has been limited progress in therapies that address the underlying causes of COPD pathogenesis. Recent studies have identified specific changes in the gut and pulmonary microbiota in response to exposure to smoke that can cause or exacerbate CS-COPD by regulating the inflammatory immune response in the lungs through the gut-lung axis. As a convenient and controllable intervention, modifying the diet to include more dietary fiber can effectively improve the prognosis of CS-COPD. Gut microbiota ferment dietary fiber to produce short-chain fatty acids, which connect the microbial communities in the lung and gut mucosa across the gut-lung axis, playing an anti-inflammatory and immunosuppressive role in the lungs. Given that the effect of dietary fiber on gut microbiota was highly similar to that of quitting smoking on gut microbiota, we assume that microbiota might be a potential therapeutic target for dietary fiber to alleviate and prevent CS-COPD. This study examines the similarities between pulmonary and gut microbiota changes in the presence of smoking and dietary fiber. It also highlights the mechanism by which SCFAs link pulmonary and gut microbiota in CS-COPD and analyzes the anti-inflammatory and immunomodulatory effects of short-chain fatty acids on CS-COPD via the gut-lung axis.
