ALLERGIC asthma remains the predominant asthma phenotype worldwide, imposing a substantial clinical and economic burden. Prevalence patterns are uneven: rates have stabilised in many high-income settings yet continue to climb across low- and middle-income countries, reflecting environmental and socioeconomic pressures. Clinically, the condition features airway hyperresponsiveness with episodic dyspnoea, non-productive cough and chest tightness, and symptom intensity typically mirrors allergen exposure. Multimorbidity is common; large proportions of patients also live with allergic rhinitis and atopic dermatitis, compounding disease severity and eroding quality of life.
Against this backdrop, the gut–lung axis has emerged as a persuasive framework for understanding disease heterogeneity. The gut microbiota, a densely populated, compositionally diverse ecosystem exceeding 10¹⁴ microorganisms, supports host homoeostasis via nutrient processing, xenobiotic metabolism and epithelial-barrier fortification. When this community tips into imbalance, systemic immune consequences follow. Three themes have crystallised. First, gut microbiota composition in allergic asthma often shows reduced diversity and shifts in key taxa, including bifidobacteria. Second, the biological activity of microbial metabolites, particularly short-chain fatty acids and tryptophan derivatives, exerts distal effects through circulation and vagal signalling, engaging G-protein-coupled receptors to promote regulatory T-cell differentiation and temper type-2 inflammation. Third, the interaction between gut microbes and the immune system shapes T-cell fate decisions; dysbiosis can skew Th2/Th17–Treg balance, weakening antiviral defences and predisposing to exacerbations.
Mechanistic studies extend these concepts, implicating oxidative stress, epithelial barrier perturbation and altered antigen presentation in the airways as downstream consequences of intestinal microbial shifts. These insights are informing intervention strategies based on microbiota modulation. Probiotics, prebiotics, synbiotics, postbiotics and targeted dietary patterns show early promise in restoring metabolite profiles, re-balancing effector and regulatory responses, and reducing symptom burden. Precision approaches may ultimately tailor strain selection and dosing to an individual’s baseline microbiome, diet, environment and genetics.
Important caveats remain. Associations do not prove causation; strain-level functions vary within a species; and many human studies are cross-sectional with short follow-up and heterogeneous endpoints. Field-advancing priorities include gnotobiotic and human challenge models to map causal pathways, large multi-omics cohorts to derive predictive signatures, and rigorously designed, strain-resolved randomised trials. Taken together, current evidence positions the microbiota as both biomarker and modifiable driver of allergic asthma, opening a path to preventive and personalised care that delivers durable control with fewer systemic side-effects.
Reference
Lv J et al. Gut-lung axis in allergic asthma: microbiota-driven immune dysregulation and therapeutic strategies. Front Pharmacol. 2025;16:1617546.
