Abstract
<b>Background:</b> Asthma is characterized by an aggravated immune response to respiratory viral infections: This phenomenon is a clinically well-recognized driver of acute exacerbations, but how different phenotypes of asthma respond immunologically to virus is unclear. <b>Objectives:</b> To describe the association between different phenotypes and severity of asthma and bronchial epithelial immune responses to viral stimulation. <b>Methods:</b> In the Immunoreact study, healthy subjects (n=10) and 50 patients with asthma were included; 30 (60%) were atopic, and 34 (68%) were eosinophilic; 15 (25%) had severe asthma. All participants underwent bronchoscopy with collection of bronchial brushings. Bronchial epithelial cells (BECs) were expanded and stimulated with the viral replication mimic poly (I:C) (TLR3 agonist) in vitro. The expression of TLR3-induced pro-inflammatory and anti-viral responses of BECs were analyzed using RT-qPCR and multiplex ELISA and compared across asthma phenotypes and severity of disease. <b>Results:</b> Patients with atopic asthma had increased production of IL-4, IFN-β, IL-6, TNF-α, and IL-1β after poly (I:C) stimulation compared to non-atopic patients, whereas patients with eosinophilic asthma and non-eosinophilic asthma did not differ in the response to poly (I:C). Patients with severe asthma displayed a decreased antiviral IFN-b, and increased expression of IL-8, most pronounced in atopic and eosinophilic asthmatics. Interestingly, release of IL-33 and TSLP in response to poly (I:C) was increased in severe eosinophilic asthma, but not in severe atopic asthma. <b>Conclusions:</b> The bronchial epithelial immune response to a viral mimic stimulation differs between asthma phenotypes and severeties.
Published Version
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