Respiratory Syncytial Virus exacerbates acute lung damage during ovalbumin-induced asthmatic inflammation

Abstract

Abstract With more than 235 million people affected, asthma is the most common chronic disease in the world. In addition, respiratory viral infections, particularly respiratory syncytial virus (RSV) infection, has been associated with asthma development and significant exacerbation of asthmatic symptoms. While there are several theories exploring the causal role of RSV infection in asthma development, the pathogenic mechanism underlying the effect of RSV on asthma exacerbation remains to be understood. In this study, we investigated the effects of RSV infection on airway immune responses and lung damage in ovalbumin (OVA)-induced asthmatic mice. We found that RSV infection exacerbates acute lung damage in asthmatic mice, as indicated by their significantly increased protein and LDH levels in the airway. Although asthma is considered an allergic disease with increased Th2 responses, the levels of IL-4 and IL-5, as well as eosinophil recruitment, were unaffected in OVA-induced asthmatic mice with or without RSV super-infection. Moreover, pro-inflammatory responses, such as TNF-alpha, KC and MIP-2 production, and neutrophil infiltration, were also comparable between RSV-infected asthmatic mice and controls that only received RSV infection. Interestingly, the number of resident alveolar macrophages significantly decreased in RSV-infected asthmatic mice, as compared with RSV-infected non-asthmatic and uninfected asthmatic controls. Considering the crucial role of alveolar macrophages in resolution of airway inflammation, our future studies will determine whether RSV impairs alveolar macrophage self-maintenance, thereby prolonging airway inflammation and exacerbating lung damage during asthma.