ArticleAllergy2022
House dust mite sensitization and exposure affects bronchial epithelial anti-microbial response to viral stimuli in patients with asthma.
Article in Allergy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 22 citations in OpenAlex.
- Allergen Immunotherapy Enhances Airway Epithelial Antiviral Immunity in Patients with Allergic Asthma (VITAL Study): A Double-Blind Randomized Controlled Trial.American journal of respiratory and critical care medicine · 2023Trial
- Quorum sensing geneFrontiers in microbiology · 2026Article
- Neighborhood disadvantage and the back-to-school epidemic of viral-associated asthma exacerbations.The Journal of allergy and clinical immunology · 2025Article
- Unraveling the mechanisms of virus-induced asthma exacerbation: epithelial injury, immune dysregulation, and novel interventions.Chinese medical journal pulmonary and critical care medicine · 2025Review
- Article
- Indoor allergen exposure and its association to upper respiratory infections and pulmonary outcomes among children with asthma.The Journal of allergy and clinical immunology · 2024Article
- The epithelial era of asthma research: knowledge gaps and future direction for patient care.European respiratory review : an official journal of the European Respiratory Society · 2024Review
- Difficult-to-treat asthma patients from ethnic minority groups in central England are at an enhanced risk of house dust mite sensitisation.Clinical and translational allergy · 2023Article
- Reply to Sokolowska and Radzikowska.American journal of respiratory and critical care medicine · 2023Article
- Molecular sensitization pattern to house dust mites is formed from the first years of life and includes group 1, 2, Der p 23, Der p 5, Der p 7 and Der p 21 allergens.Clinical and molecular allergy : CMA · 2023Article
- Article
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionAllergen exposure worsens viral-triggered asthma exacerbations and could predispose the host to secondary bacterial infections. We have previously demonstrated that exposure to house dust mite (HDM) reduced TLR-3-induced IFN-β in human bronchial epithelial cells (HBECs) from healthy donors. We hypothesize that HDM sensitization in different ways may be involved in both viral and bacterial resistance of HBECs in asthma. In this study, the role of HDM sensitization and effects of HDM exposure on viral stimulus-challenged HBECs from asthmatic donors have been explored with regard to expression and release of molecules involved in anti-viral and anti-bacterial responses, respectively.
methodsHBECs from HDM-sensitized (HDM+) and unsensitized (HDM-) patients with asthma were used. HBECs were exposed to HDM or heat inactivated (hi)-HDM (20 μg/ml) for 24 h prior to stimulation with the viral infection mimic, Poly(I:C), for 3 or 24 h. Samples were analyzed with ELISA and RT-qPCR for β-defensin-2, IFN-β, TSLP, and neutrophil-recruiting mediators: IL-8 and TNF-⍺. NFκB signaling proteins p105, p65, and IκB-⍺ were analyzed by Western blot.
resultsPoly(I:C)-induced IFN-β expression was reduced in HBECs from HDM + compared to HDM- patients (p = 0.05). In vitro exposure of HBECs to HDM furthermore reduced anti-microbial responses to Poly(I:C) including β-defensin-2, IL-8, and TNF-⍺, along with reduced NFκB activity. This was observed in HBECs from asthma patients sensitized to HDM, as well as in non-sensitized patients. By contrast, Poly (I:C)-induced release of TSLP, a driver of T2 inflammation, was not reduced with exposure to HDM.
conclusionUsing HBECs challenged with viral infection mimic, Poly(I:C), we demonstrated that allergic sensitization to HDM was associated with impaired anti-viral immunity and that HDM exposure reduced anti-viral and anti-bacterial defense molecules, but not TSLP, across non-allergic as well as allergic asthma. These data suggest a role of HDM in the pathogenesis of asthma exacerbations evoked by viral infections including sequential viral-bacterial and viral-viral infections.
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