Abstract

Abstract Acute viral infections are the most frequent cause of asthma exacerbations, and are therefore responsible for the majority of healthcare costs attributed to asthma. Human rhinovirus is the most common identified one in children and adults. It has been shown that IL-33- driven mechanism initiates TH2 responses to the clinically relevant allergens house dust mite (HDM). We have shown that TSLP is increased in asthma exacerbation. Alveolar macrophages have higher expression of IL-33 and TSLP in asthma. To determine whether HDM can have an effect on IL-33 and TSLP gene expression in response to human rhinovirus (RV), we treated bone marrow-derived macrophages (BMM) with HDM in the presence of M-CSF and infected them with RV1B. RV1B induced expression of IL-33 (2-fold, P-value<0.001) and TSLP (2-fold P-value<0.05) in HDM- treated macrophages after 24 hours compared to HDM non-treated BMM. RV1B infection caused an increase in IL-33 in IL-33 (P-value<0.01) and TSLP ( P-value<0.01) in HDM treated BMM compared to UV-treated RV1B group. There was no increase in IL-33 and TSLP gene expression in response to RV1B in the HDM-treated BMM at eight hours compared to UV-treated RV1B group, while HDM non-treated BMM showed increase in IL-33 (P-value<0.01) and TSLP (P-value=0.059 ) in response to RV1B compared to UV-treated RV1B. These results suggest that HDM increases IL-33 and TSLP gene expression in macrophages in response to RV1B which can play a role in asthma exacerbations.

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