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Updated: Mar 14, 2026

Symptom Assessment of Patients with Allergic Rhinitis Using an Allergen Exposure Chamber
Published on: March 3, 2023
Preservation of epithelial cell barrier function and muted inflammation in resistance to allergic rhinoconjunctivitis
Sunil K Ahuja1, Muthu Saravanan Manoharan2, Nathan L Harper3
1Veterans Administration Center for Personalized Medicine, South Texas Veterans Health Care System, San Antonio, Tex; Department of Medicine, University of Texas Health Science Center, San Antonio, Tex; Department of Microbiology and Immunology, University of Texas Health Science Center, San Antonio, Tex; Department of Biochemistry, University of Texas Health Science Center, San Antonio, Tex.
Background:
An emerging paradigm holds that resistance to the development of allergic diseases, including allergic rhinoconjunctivitis, relates to an intact epithelial/epidermal barrier during early childhood. Conceivably, the immunologic and genomic footprint of this resistance is preserved in nonatopic, nonallergic adults and is unmasked during exposure to an aeroallergen.
Objective:
The aim of this study was to obtain direct support of the epithelial/epidermal barrier model for allergic rhinoconjunctivitis.
Methods:
Twenty-three adults allergic to house dust mites (HDMs) (M+) and 15 nonsensitive, nonallergic (M-) participants completed 3-hour exposures to aerosolized HDM (Dermatophagoides pteronyssinus) powder on 4 consecutive days in an allergen challenge chamber. We analyzed: (1) peripheral blood leukocyte levels and immune responses; and (2) RNA sequencing-derived expression profiles of nasal cells, before and after HDM exposure.
Results:
On HDM challenge: (1) only M+ persons developed allergic rhinoconjunctivitis symptoms; and (2) peripheral blood leukocyte levels/responses and gene expression patterns in nasal cells were largely concordant between M+ and M- participants; gross differences in these parameters were not observed at baseline (pre-exposure). Two key differences were observed. First, peripheral blood CD4+ and CD8+ T-cell activation levels initially decreased in M- participants versus increased in M+ participants. Second, in M- compared with M+ participants, genes that promoted epidermal/epithelial barrier function (eg, filament-aggregating protein [filaggrin]) versus inflammation (eg, chemokines) and innate immunity (interferon) were upregulated versus muted, respectively.
Conclusion:
An imprint of resistance to HDM challenge in nonatopic, nonallergic adults was muted T-cell activation in the peripheral blood and inflammatory response in the nasal compartment, coupled with upregulation of genes that promote epidermal/epithelial cell barrier function.
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