ArticleJournal of asthma and allergy2026
Unique Associations Between Complement Split Products and Pollen Species in Adults with Respiratory Allergic Disease: A Pilot Study.
Article in Journal of asthma and allergy, 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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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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7 authors.
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Abstract
Background: Complement split product (CSP) anaphylatoxins, C3a and C5a, are important mediators of innate immune responses and have been implicated in the pathogenesis of asthma. Environmental pollen exposure is a trigger of asthma symptoms, leading to generation of CSP, which amplify allergic responses. The relationship between seasonal pollen levels, complement activation and clinical outcomes of asthma control remain unknown. This exploratory pilot study evaluated the association between concurrent tree, grass, and weed pollen exposure, CSP levels, and measures of asthma control in adults with asthma. Methods: In this prospective study, which included 11 allergic adults, blood samples were drawn monthly for measurement of plasma C5a desArg and C3a desArg levels (ELISA). Concurrent local tree, grass, and weed pollen exposure, as well as clinical measures of asthma control (ACT) were determined. Spearman correlation matrices were computed. Results: Tree pollen counts were positively associated with C3a desArg expression (r=0.562, p<0.0001). Weed pollen counts were negatively associated with C3a desArg expression (r=-0.419, p<0.0001). Increasing weed pollen counts decreased FeNO (β=0.956, p<0.001). Higher C5a desArg levels over time correlated with increased ACT scores (p=0.02), improved AQLQ and RQLQ (P=0.03, 0.03, respectively). Conclusion: Seasonal pollen exposure is associated with distinct patterns of complement activation in asthma. Larger studies are required to elucidate the relation of these patterns of complement activation to immune mechanisms in asthma pathogenesis and clinical disease.
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