Abstract
Acute viral infections are the most frequent cause of asthma exacerbation, and are the major cause for morbidity, mortality, and healthcare costs associated with asthma. Human rhinovirus is the most common identified responsible virus 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 thymic stromal lymphopoietin (TSLP) is increased in a murine viral-induced asthma exacerbation model. Alveolar macrophages have a 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 (BMMs) 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 BMMs after 24 hours compared to HDM non-treated BMMs. RV1B infection caused an increase in IL-33 (2.2-fold, P-value<0.01) and TSLP (2.1-fold, P-value<0.01) in HDM treated BMMs compared to UV-treated RV1B infected BMMs. There was no increase in IL-33 and TSLP gene expression in response to RV1B in the HDM-treated macrophages at eight hours compared to UV-treated RV1B group, while HDM non-treated BMMs 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 BMMs in response to RV1B. This response is delayed compared to HDM non-treated BMMs. The increase in IL-33 and TSLP can play a role in asthma exacerbations.
- © 2014 ERS