Gut-lung axis in chronic respiratory diseases: a narrative review of emerging insights.

Background and Objective: The gut-lung axis is a bidirectional network through which intestinal microbial ecology, mucosal immunity, epithelial barrier function, microbial metabolites, and neurohumoral signalling influence pulmonary inflammation. This narrative review summarizes the mechanistic basis of gut-lung communication, compares the strength of evidence across major chronic respiratory diseases (CRDs), and evaluates emerging microbiome-targeted interventions. Methods: PubMed, Embase, and Google Scholar were searched for peer-reviewed English-language literature published from January 2010 through June 2024 using combinations of terms related to the gut-lung axis, microbiome, asthma, chronic obstructive pulmonary disease (COPD), interstitial lung disease (ILD), short-chain fatty acids (SCFAs), intestinal permeability, bile acids, tryptophan metabolites, vagal signalling, and glucagon-like peptide-1 (GLP-1). Human and animal original studies, randomized trials, cohort studies, mechanistic studies, and relevant narrative or systematic reviews were considered; case reports, non-English articles, and studies without respiratory outcomes were excluded. Reference lists of key papers were also hand-searched. Key Content and Findings: Evidence is strongest for biologically plausible immune and metabolic pathways linking intestinal dysbiosis to pulmonary disease. In asthma, early-life depletion of SCFA-producing taxa may impair regulatory T-cell development and promote allergic sensitization. In COPD, gut dysbiosis, increased intestinal permeability, and systemic endotoxin exposure are more consistently associated with inflammatory phenotype and exacerbation burden. Evidence in ILD remains preliminary but supports a possible role for gut-derived pathogen-associated molecular patterns in profibrotic signalling. After lung transplantation (LT), antibiotic exposure, immunosuppression, and microbial loss may interact with allograft inflammation and chronic lung allograft dysfunction (CLAD). Dietary modulation, probiotics, prebiotics/synbiotics, post-biotics, and fecal microbiota transplantation (FMT) remain investigational, with heterogeneous and generally limited clinical evidence. Conclusions: Current data support mechanistic plausibility but do not justify routine microbiome-directed treatment of CRDs. Future trials should standardize microbiome profiling, incorporate metabolomic and disease-specific clinical endpoints, and stratify responders to define where gut-lung axis interventions can add clinically meaningful benefit.