ReviewFrontiers in allergy2026
The nasal-oral microbiome axis in allergic rhinitis: environmental triggers, microbial dysbiosis, and immune dysregulation.
Review in Frontiers in allergy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Metformin as an Innate Immune Modulator: Metabolic and Epigenetic Reprogramming of Innate Immune Cells and Therapeutic Implications.Current issues in molecular biology · 2026Review
- Supragingival plaque microbiome features in allergic rhinitis and allergic asthma and their association with dental caries: a cross-sectional study.Journal of oral microbiology · 2026Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Allergic rhinitis (AR) is a common chronic inflammatory disease, which affects about 400 million people around the world. The role of the upper airway microbiota in the development of AR has recently emerged and seems to be an important player in its pathology, but there are still no detailed mechanistic models that incorporate exposure to the environment, dysbiosis of microbes or dysregulated immunity as a whole. In this review we summarize the state of the art about the microbiome nose-mouth connection in AR to understand how environmental stimuli change the microbiota composition as well as how an imbalance can induce allergy-related inflammation. This review follows a narrative approach. Literature was identified through systematic searches of PubMed, Web of Science, and Scopus databases (up to March 2025) using the following key terms and their combinations: "allergic rhinitis', "nasal microbiome", "oral microbiome", "dysbiosis", "epithelial barrier", 'short-chain fatty acids', "Th2 inflammation", and "probiotics". Inclusion criteria encompassed original research articles, systematic reviews, and meta-analyses published in English; conference abstracts, case reports, and purely non-human studies were excluded unless they provided mechanistic insights not available from human data. Environmental exposures substantially alter upper airway microbial communities. Air pollutants such as PM₂.₅ and diesel exhaust particles (DEP) damage epithelial tight junction proteins via reactive oxygen species (ROS), increasing nasal permeability. DEP additionally functions as an immune adjuvant by promoting pro-Th2 immune polarization. Antibiotic treatment during early childhood may affect GI tract development by altering resident bacterial populations, being considered as a strong risk factor for developing AR. On the other hand, farm exposure and microbial diversity provide protection by enhancing regulatory T cell induction. AR patients exhibit characteristic nasal dysbiosis, including overgrowth of Staphylococcus aureus and Moraxella catarrhalis alongside depletion of protective commensals such as Dolosigranulum pigrum and Corynebacterium spp. This dysbiosis disrupts the epithelial barrier, triggering alarmin release (TSLP, IL-25, IL-33) and amplifying type 2 inflammation. The oral microbiota also contributes via the oral-nasal-pulmonar
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