SynthesisFrontiers in pharmacology2026
Systematic review and meta-analysis of the effects of air pollution exposure on nasal mucosal immune-inflammatory markers in experimental animal models of AR.
Synthesis in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Although air pollution is associated with the onset and exacerbation of allergic rhinitis (AR), epidemiological studies alone cannot reveal the tissue-level immune mechanisms because factors such as the strength of exposure, duration of exposure, presence of co-pollutants and individual susceptibility are all difficult to control. Experiments on animals have provided support for research on the immune response in the nasal mucosa under controlled conditions. A systematic review and meta-analysis were conducted to quantify changes in nasal mucosal immune-inflammatory markers and to assess the strength of mechanistic evidence from various experiments. According to PRISMA, PubMed, Web of Science, Embase and the Cochrane Library were searched from the beginning until December 2025. Eighteen eligible rodent studies were included. As the primary outcomes, type 2 inflammation-related markers were selected because they had been reported frequently and were biologically central to asthma (asthma/AR), such as eosinophils, IL-4, IL-5, IL-13 and OVA-specific IgE. Other markers included ZO-1, NLRP3, IL-1β, IL-17, IL-33, IFN-γ, neutrophils, lymphocytes and total IgE, and were used as secondary or exploratory outcomes. Pooled effects were expressed as standardised mean differences (SMDs) with 95% confidence intervals, and a random-effects model was used. Exposure to air pollutants was associated with an increase in eosinophils, elevated IL-4, IL-5, IL-13, and OVA-specific IgE; thus, a type 2 inflammatory response had been enhanced. A few studies have also indicated that there may be defects in the epithelial barrier and activation of the innate immune system, as shown by reduced ZO-1 and increased IL-1β/NLRP3. The available evidence did not show a consistent effect on IFN-γ expression. Due to considerable heterogeneity and a lack of mechanistic markers for some other reasons, these results should be interpreted cautiously and are not considered definitive causal pathways.
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