Gut and respiratory microbiomes in asthma and allergic diseases: a narrative review of mechanistic insights, gut-lung axis interactions and therapeutic opportunities

Introduction

Background

Asthma and allergic diseases are among the most prevalent chronic inflammatory disorders worldwide and represent a growing public health burden across both pediatric and adult populations. Their incidence has risen substantially over recent decades, especially in industrialized and urbanized regions, indicating that environmental and lifestyle-related factors contribute importantly to disease susceptibility beyond genetic predisposition (1-3). Asthma is characterized by chronic airway inflammation, airway hyperresponsiveness, and variable airflow limitation, whereas allergic diseases such as allergic rhinitis, atopic dermatitis, and food allergy are marked by immune dysregulation, epithelial barrier dysfunction, and exaggerated responses to otherwise harmless antigens (1,2). Although these conditions affect different target organs, they share common immunopathological features, including type 2 inflammation, impaired immune tolerance, and persistent mucosal barrier abnormalities.

Traditional models of asthma and allergy pathogenesis have focused on gene-environment interactions, allergen exposure, respiratory infections, pollution, and host immune immaturity. The hygiene hypothesis and related concepts propose that reduced microbial exposure during early life may impair immune education and favor allergic sensitization (1,3,4). Within this framework, the human microbiome has emerged as a critical mediator linking environmental exposures to immune development and disease risk.

The gut microbiome and respiratory microbiome are now recognized as two major microbial ecosystems involved in host homeostasis and immune regulation (3,5,6). Disruption of these ecological networks, commonly described as dysbiosis, has been associated with asthma susceptibility, allergic sensitization, disease severity, and exacerbation risk (1,3,6). Microbial metabolites, including short-chain fatty acids, tryptophan-derived metabolites, and bile acid derivatives, can influence epithelial integrity, dendritic cell activity, T-cell differentiation, and inflammatory signaling pathways (7-11). At the same time, growing evidence supports the concept of a bidirectional gut-lung axis, whereby gut-derived microbial products and immune signals may affect distal respiratory immunity, while airway inflammation, respiratory infection, medication exposure, and systemic immune activation may also feed back on intestinal microbial ecology (12-16).

Knowledge gap

Despite the rapid expansion of microbiome research in asthma and allergic diseases, several important limitations remain. Many studies have examined the gut microbiome and respiratory microbiome separately, resulting in a fragmented understanding of their relative and combined contributions to disease pathogenesis (3,5,6). Much of the existing literature remains associative rather than mechanistic, and microbial signatures identified in human cohorts do not necessarily establish causality (3,5,6,10,17). Conversely, many detailed mechanistic insights come from animal or in vitro models and require cautious translation to human disease. In addition, the biological components of the gut-lung axis are still not fully resolved (12-15,18). Clinical translation remains limited because results from probiotics, prebiotics, dietary interventions, and fecal microbiota transplantation have been inconsistent and are complicated by methodological heterogeneity (19-33).

Objective and scope of this review

This review provides a comprehensive and mechanistically oriented overview of the roles of the gut and respiratory microbiomes in the pathogenesis and progression of asthma and allergic diseases. It summarizes microbiome alterations associated with disease (3-5,34,35), examines how microbial communities influence allergic inflammation (7-13,36), discusses the gut-lung axis as an integrative framework (12-16), and evaluates current and emerging microbiome-targeted strategies (15,19-25,28,37,38). We present this article in accordance with the Narrative Review reporting checklist (available at https://tp.amegroups.com/article/view/10.21037/tp-2026-0360/rc).

Methods

This article was designed as a narrative review rather than a systematic review or meta-analysis. We searched PubMed, Web of Science, and Google Scholar for English-language literature published from January 2010 to February 2026 using combinations of terms related to asthma, allergic diseases, gut microbiome, respiratory microbiome, gut-lung axis. Reference lists of relevant reviews and key mechanistic articles were also screened. Studies were selected for relevance to microbiome alterations, mechanistic plausibility, gut-lung axis biology, and translational strategies. Because the aim was interpretive synthesis rather than quantitative evidence pooling, formal risk-of-bias scoring, meta-analysis, and PRISMA-style study selection were not performed. Table 1 summarizes the narrative literature search and selection approach.

Microbiome alterations associated with asthma and allergic diseases

Early-life gut microbiome colonization and allergic susceptibility

Early life represents a critical developmental window during which gut microbial development appears to shape immune maturation and later allergic susceptibility. Human birth-cohort studies consistently associate delivery mode, feeding practices, maternal microbial transfer, antibiotic exposure, infection history, and environmental microbial diversity with infant gut microbial composition and later asthma or allergy risk (3,4,34,39). However, these data are largely associative and may be confounded by host genetics, antibiotic indication, diet, environment, and socioeconomic factors. Mechanistic support comes mainly from experimental studies showing that disrupted microbial succession can alter dendritic cell maturation, regulatory T-cell induction, Th2-skewed immunity, and microbial metabolite production (1,7,8,36). Thus, early-life dysbiosis should be interpreted as a marker and potential contributor to immune deviation rather than as a single deterministic cause of allergic disease, as shown in Table 2.

Respiratory microbiome dysbiosis and disease phenotypes

The respiratory microbiome is increasingly recognized as an important determinant of airway immune homeostasis and asthma-related disease expression. Human airway studies show that asthma and allergic airway disease are often associated with reduced microbial diversity and enrichment of potentially pathogenic genera such as Haemophilus, Moraxella, Streptococcus, and Neisseria (5,6,17). Unlike the gut microbiome, which is often linked to systemic immune education and metabolite-mediated signaling, the respiratory microbiome is positioned at the site of airway inflammation and may be more directly related to local epithelial activation, neutrophilic inflammation, infection susceptibility, and exacerbation tendency (17,35,42,43). Nevertheless, whether airway dysbiosis initiates disease, reflects inflamed airway ecology, or both, remains context dependent.

Shared and site-specific microbial signatures in asthma and allergic diseases

A useful framework is to distinguish shared dysbiosis features from site-specific functions. Both gut and respiratory microbiomes may show reduced diversity, loss of beneficial commensals, and enrichment of taxa associated with inflammation or impaired barrier function (3,5,6). The gut microbiome is most strongly linked to early immune education, systemic tolerance, metabolic outputs, and circulating immunomodulatory molecules, whereas the respiratory microbiome is more closely linked to local airway ecology, inflammatory phenotype, infection-exacerbation dynamics, and airway remodeling (3,5,11,17). This distinction helps separate systemic developmental effects from local airway effects and provides a clearer basis for interpreting gut-lung axis interactions, as shown in Table 3.

Mechanistic links between the microbiome and allergic inflammation

Microbiome-immune crosstalk in gut and airway mucosa

The microbiome influences allergic disease through overlapping immune pathways in the gut and airways. In human studies, altered gut and airway microbial patterns are associated with allergic sensitization, asthma phenotype, and disease severity, but these associations do not by themselves prove causality (3,5,6,17). Mechanistic evidence, mainly from animal and cellular studies, suggests that commensal microorganisms can shape dendritic cell maturation, promote regulatory T-cell development, influence T helper cell type 1/T helper cell type 2 (Th1/Th2) balance, and modulate epithelial cytokine signaling (7,11,36). In the airways, the respiratory microbiome is not simply a downstream marker of gut dysbiosis; it may directly interact with epithelial cells, macrophages, neutrophils, and pattern-recognition receptors to influence local cytokine release, mucus production, antimicrobial defense, and eosinophilic or neutrophilic inflammation (6,17,46). Thus, microbiome-immune crosstalk should be interpreted as a set of local and systemic mechanisms supported by different levels of evidence across experimental and human settings.

Microbial metabolites and downstream immune regulation

Short-chain fatty acids and regulatory immune responses

Among microbial metabolites, short-chain fatty acids are the most extensively studied in relation to asthma and allergic diseases. Human observational studies link reduced SCFA-producing taxa or altered metabolite profiles with asthma risk and disease severity, whereas experimental studies provide stronger mechanistic support for acetate, propionate, and butyrate in promoting regulatory T-cell development, supporting epithelial integrity, and suppressing excessive inflammatory signaling (7,8,13). SCFAs may influence the lung both indirectly through systemic immune regulation and directly through effects on airway epithelial and immune-cell responses after entering the circulation. However, the degree to which circulating SCFAs determine clinical asthma phenotypes in humans remains incompletely established (7,10,13).

Tryptophan metabolites, bile acids, and other signaling mediators

Tryptophan metabolites and bile-acid derivatives illustrate a broader principle: microbiome function may be more informative than taxonomy alone. Microbial tryptophan metabolites can activate the aryl hydrocarbon receptor and influence mucosal immune homeostasis, while microbially modified bile acids interact with host receptors such as farnesoid X receptor (FXR) and Takeda G protein-coupled receptor 5 (TGR5) to modulate inflammatory and metabolic regulation (7,9,11). These pathways are mechanistically plausible, but direct human evidence linking specific metabolite changes to asthma onset, phenotype stability, or treatment response remains emerging.

Epithelial barrier dysfunction, inflammatory signaling, and epigenetic regulation

Epithelial barrier dysfunction is a central feature linking microbiome disturbance to asthma and allergic diseases. Human studies support the coexistence of barrier impairment, dysbiosis, and allergic inflammation, while experimental models suggest that dysbiosis may weaken tight junction integrity, increase permeability, and facilitate abnormal exposure to allergens and pathogens (2,6,36). In the respiratory tract, airway dysbiosis may further amplify epithelial alarmin release, mucus hypersecretion, impaired antimicrobial defense, and susceptibility to viral infection. Viral infections such as respiratory syncytial virus and rhinovirus can in turn alter airway microbial communities and intensify inflammatory signaling, creating a local feedback loop between the respiratory microbiome and airway inflammation (44,45,47-50). In parallel, microbial metabolites such as SCFAs can affect histone deacetylase activity and other epigenetic pathways, thereby exerting longer-term effects on immune programming (7,8,51). These mechanisms are best viewed as interacting pathways rather than isolated linear causal chains, as shown in Table 4.

The gut-lung axis in disease initiation and progression

Biological basis of the gut-lung axis

The gut-lung axis refers to the bidirectional biological communication between the intestinal microbiome and the respiratory system (12-16). The gut and lung are connected through systemic immune pathways, circulating microbial metabolites, and shared inflammatory networks. This framework helps explain how microbial events in the gut can influence airway immunity and how respiratory inflammation may affect intestinal microbial homeostasis, as shown in Figure 1.

Figure 1 Schematic overview of the gut-lung axis in asthma and allergic diseases. The gut-lung axis is bidirectional. Gut dysbiosis may influence the respiratory system through immune-cell trafficking, systemic immune education, and circulating microbial metabolites. Conversely, airway dysbiosis, respiratory infection, airway inflammation, hypoxia, corticosteroid or antibiotic exposure, and systemic inflammatory responses may feed back on intestinal microbial composition and barrier function. These reciprocal pathways contribute to allergic inflammation, viral susceptibility, exacerbations, and airway remodeling.

Immune cell trafficking and systemic immune education

One direction of the gut-lung axis involves intestinal immune education and immune-cell trafficking to distant mucosal sites. Immune cells conditioned in the intestinal mucosa may later migrate to the lungs, shaping the balance between tolerance and inflammation (12,14,18,36). Gut dysbiosis may therefore alter distal airway immune responses by modifying mucosal priming, systemic immune-cell development, and circulating metabolite exposure.

Circulating microbial metabolites and distal organ effects

The reverse direction of the gut-lung axis is equally important. Airway dysbiosis, respiratory viral infection, chronic airway inflammation, and asthma therapies may influence systemic immune tone, swallowing of airway secretions, intestinal permeability, and antimicrobial or corticosteroid exposure, all of which can reshape intestinal microbial ecology (12-16,44,45,47-50). This bidirectional model avoids treating asthma as a simple consequence of gut dysbiosis and better reflects the contribution of the respiratory microbiome highlighted in the title of this review.

Contribution of the gut-lung axis to asthma progression

Airway inflammation and immune imbalance

The gut-lung axis is increasingly recognized as an important contributor to asthma progression because it integrates systemic immune programming with local airway inflammation. Gut dysbiosis may reduce immunoregulatory metabolites and alter immune priming, whereas airway dysbiosis may directly shape epithelial activation, mucus production, neutrophilic or eosinophilic inflammation, and infection susceptibility (7,8,12,13,15-17,36,42). These reciprocal effects may influence disease onset, severity, persistence, and inflammatory phenotype.

Viral interactions, exacerbations, and airway remodeling

Respiratory viral infections, acute exacerbations, and airway remodeling further illustrate why the axis should be considered bidirectional. Viral infections such as respiratory syncytial virus and rhinovirus are major triggers of asthma attacks, and airway microbial shifts may impair antiviral immunity or amplify inflammation (44,45,47-50). At the same time, systemic inflammation and treatment exposures during exacerbations may perturb gut microbial communities. Persistent microbiome-related immune dysregulation may contribute to epithelial injury, mucus hypersecretion, and structural airway changes (12,52,53).

Microbiome-targeted prevention and therapeutic strategies

Probiotics, prebiotics, and synbiotics

Preventive use in early life

Probiotics, prebiotics, and synbiotics have attracted substantial interest as early-life strategies to reduce allergic disease risk by modulating microbial colonization during a critical window of immune development (19-24). The most consistent clinical signal is for eczema prevention, whereas evidence for asthma prevention remains weaker and more inconsistent (19,20,23). These differences likely reflect strain specificity, timing, baseline microbiome composition, host diet, and heterogeneity in outcome definitions.

Therapeutic use in established disease

For established disease, probiotics and related interventions should be viewed as adjunctive and evidence-limited rather than established asthma therapies. Some studies suggest improvement in allergic rhinitis symptoms, but asthma outcomes remain mixed and depend on strain selection, treatment duration, age, phenotype, and concomitant therapy (21-26). Current evidence does not support treating all probiotic, prebiotic, and synbiotic strategies as equivalent.

Dietary modulation and metabolite-oriented interventions

Dietary modulation has a stronger biological rationale than many intensive microbiome interventions because diet can influence microbial substrate availability and metabolite production. High-fiber diets and microbiome-supportive dietary patterns may enhance SCFA production, strengthen epithelial barrier function, and reduce inflammatory signaling (54-57). However, clinical responses vary across individuals and likely depend on baseline microbiome composition, dietary adherence, host metabolism, and disease phenotype (58,59). Dietary strategies are therefore promising but still require better phenotype-specific evidence.

Fecal microbiota transplantation and emerging microbiome-based therapies

Fecal microbiota transplantation and next-generation microbiome therapies should be separated from probiotics and diet because their evidence base is much less mature for asthma and allergic diseases. Fecal microbiota transplantation has shown promise mainly in preclinical allergic airway inflammation models, but clinical evidence remains limited and important concerns persist regarding donor selection, safety, reproducibility, durability, and regulatory oversight (15,28,37,38). Emerging next-generation probiotics, targeted microbial consortia, metabolite-based therapies, and precision microbiome approaches remain largely conceptual or early translational strategies that require validated biomarkers and prospective clinical testing (15,28,60).

Current limitations in clinical translation

Translation into routine clinical practice remains limited because the evidence base is uneven across intervention types. Preventive probiotic strategies have some clinical signal, particularly for eczema; asthma prevention and treatment results remain inconsistent; dietary approaches are biologically plausible but heterogeneous; fecal microbiota transplantation remains mainly preclinical; and precision microbiome-based therapy is still an emerging concept (19-33,58,60,61). Future trials should stratify patients by baseline microbiome composition, disease phenotype, age, diet, medication exposure, and functional microbial readouts, as shown in Table 5 and Figure 2.

Figure 2 Microbiome-mediated mechanisms and therapeutic targets in asthma and allergic diseases. Microbiome dysbiosis, barrier dysfunction, and altered metabolite production promote immune imbalance and persistent inflammation. These mechanisms create multiple intervention points, including probiotics, prebiotics, synbiotics, dietary modulation, fecal microbiota transplantation, and precision microbiome-based therapies. LPS, lipopolysaccharide; SCFA, short-chain fatty acids.

Conclusions

Accumulating evidence indicates that the gut and respiratory microbiomes are associated with asthma and allergic diseases through effects on immune maturation, epithelial barrier integrity, inflammatory signaling, microbial metabolite production, infection susceptibility, and airway ecological stability (1,3,5,7,11). The current evidence base should be interpreted in layers: human studies support important associations between microbial patterns and disease phenotypes; longitudinal studies provide stronger temporal clues; and preclinical studies offer mechanistic plausibility. The gut microbiome appears especially relevant to immune education, systemic tolerance, and metabolite-mediated signaling, whereas the respiratory microbiome is more closely linked to local airway inflammation, infection susceptibility, exacerbation patterns, and inflammatory phenotype (3,5,11,17). The gut-lung axis is therefore best understood as a bidirectional framework integrating systemic and local microbial-immune interactions rather than as a one-way pathway from intestinal dysbiosis to asthma. Future research should focus on integrating taxonomic, functional, immunological, and clinical data, improving methodological standardization, and refining patient stratification so that microbiome-informed precision medicine can become a realistic clinical goal (29-33,60).

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the Narrative Review reporting checklist. Available at https://tp.amegroups.com/article/view/10.21037/tp-2026-0360/rc

Peer Review File: Available at https://tp.amegroups.com/article/view/10.21037/tp-2026-0360/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://tp.amegroups.com/article/view/10.21037/tp-2026-0360/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

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