Induction of IL-20 Cytokines during Viral Exacerbations of Chronic Obstructive Pulmonary Disease

Background: Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory lung disease. This pathology can be exacerbated by bacteria or viruses, such as respiratory syncytial virus (RSV). The expression of IL-20 cytokines (IL-19, IL-20, IL24) is induced by different types of infections, but also by cigarette smoke exposure. They are involved in the control of inflammation and anti-infective mechanisms. They act in many physio-pathological processes affecting different organs. Thus, an imbalance of these cytokines could be involved in the susceptibility to infections responsible for COPD exacerbations. Aim: Our goal is to define the role of IL-20 cytokines during viral exacerbations of COPD. Methods: C57/Bl6 mice are chronically exposed to cigarette smoke for 12 weeks and then infected with PVM (Pneumonia virus of mice), a murine homologue of RSV. Inflammation and IL-20 cytokines expression were assessed by histology, PCR, ELISA and flow cytometry at the pulmonary level. Results: Chronic exposure to cigarette smoke and PVM infection induce pulmonary inflammation characterized by increased expression and production of pro-inflammatory cytokines such as: CXCL-1, IFNg, massive recruitment of dendritic cells, NKT cells and CD8+ T cells. This response is associated with an early increase of IL-24 expression in cigarette smoke exposed mice. Interestingly, a defect of anti-viral defense mechanisms is observed, with lower expression of the Rsad2 gene and lower production of IL-28AB and IFNb. Conclusions: The results obtained in our experimental model show that PVM can exacerbate COPD, and that IL-20 cytokines are increased in the lung tissues.