Myeloid-associated differentiation marker is associated with type 2 asthma and is upregulated by human rhinovirus infection.

Autor:	Tanyaratsrisakul S; Asthma and Airway Disease Research Center, University of Arizona, Tucson, AZ, United States., Dy ABC; Asthma and Airway Disease Research Center, University of Arizona, Tucson, AZ, United States., Polverino F; Department of Medicine, Baylor College of Medicine, Houston, TX, United States., Numata M; Department of Medicine, National Jewish Health, Denver, CO, United States., Ledford JG; Asthma and Airway Disease Research Center, University of Arizona, Tucson, AZ, United States.; Department of Cellular and Molecular Medicine, University of Arizona, Tucson, AZ, United States.
Jazyk:	angličtina
Zdroj:	Frontiers in immunology [Front Immunol] 2023 Aug 11; Vol. 14, pp. 1237683. Date of Electronic Publication: 2023 Aug 11 (Print Publication: 2023).
DOI:	10.3389/fimmu.2023.1237683
Abstrakt:	Background: Human rhinoviruses are known to predispose infants to asthma development during childhood and are often associated with exacerbations in asthma patients. MYADM epithelial expression has been shown to associate with asthma severity. The goal of this study was to determine if MYADM expression patterns were altered in asthma and/or rhinovirus infection and if increased MYADM expression is associated with increased asthma-associated factors. Methods: Utilizing H1HeLa cells and differentiated primary human airway epithelial cells (AECs), we measured the expression of MYADM and inflammatory genes by qRT-PCR in the presence or absence of RV-1B infection or poly I:C treatment and with siRNA knockdown of MYADM. Expression of MYADM in the asthmatic lung was determined in the ovalbumin (ova)-challenged murine model. Results: MYADM expression was upregulated in the lungs from ova-treated mice and in particular on the subsurface vesicle membrane in airway epithelial cells. Upon infection with RV-1B, human AECs grown at an air-liquid interface had increased the MYADM expression predominantly detected in ciliated cells. We found that the presence of MYADM was required for expression of several inflammatory genes both in a resting state and after RV-1B or poly I:C treatments. Conclusions: Our studies show that in a mouse model of asthma and during RV-1B infection of primary human AECs, increased MYADM expression is observed. In the mouse model of asthma, MYADM expression was predominantly on the luminal side of airway epithelial cells. Additionally, MYADM expression was strongly associated with increases in inflammatory genes, which may contribute to more severe asthma and RV-linked asthma exacerbations. Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. (Copyright © 2023 Tanyaratsrisakul, Dy, Polverino, Numata and Ledford.)
Databáze:	MEDLINE
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