Nasal virus infection induces asthma exacerbation through B‐cell‐dependent recruitment of inflammatory monocytes.

Background Methods Results Conclusions Upper respiratory viral infections (URVIs) are responsible for 80% of asthma exacerbation episodes. However, the underlying mechanisms remain poorly understood.In this study, we used a mouse model of URVI and examined the impact of URVI on asthma phenotypes and the underlying mechanisms.Previously, we have reported that nasal‐restricted infection with respiratory syncytial virus (RSV) only produces mild sino‐nasal inflammation and mucus production, without causing direct lung infection. However, such nasal‐restricted infection dramatically enhanced TH2 and TH17 inflammatory responses in the lungs and increased airway hyperresponsiveness (AHR) in mice with house dust mite (HDM)‐induced asthma. Additionally, nasal‐restricted infection with RSV recruited Ly6C+ inflammatory monocytes (IMs) into the lungs of mice with and without HDM‐induced asthma. The expression of monocyte chemokines, including CCL2 and CCL7, also increased. Interestingly, nasal virus infection‐induced AHR was abolished in mice depleted of IMs and in <italic>CCR2−/−</italic> mice, indicating that the recruited IMs play a key role in nasal virus infection‐induced asthma exacerbations in mice. Lastly, we observed that recruitment of Ly6C+ IMs following URVI was abolished in mice lacking B cells and that nasal‐restricted infection with RSV increased numbers of CCL2+CCL7+ B cells in the lungs of mice as compared to controls.Taken together, our data have shown that URVI enhances the allergic inflammatory response and AHR through a B cell‒monocyte regulatory axis. [ABSTRACT FROM AUTHOR]