Tehran University of Medical Sciences Iranian Journal of Allergy, Asthma and Immunology 1735-1502 14 4 2015 10 20 392 401 EN HS Kim Department of Pediatrics, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea. H Lee Department of Pediatrics, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea. HS Kim Department of Pediatrics, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea. Sulmui Won Department of Pediatrics, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea. EK Lee Department of Pediatrics, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea. Kyongwon Bang Department of Pediatrics, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea. YH Chun Department of Pediatrics, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea. Jongseo Yoon Department of Pediatrics, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea. HH Kim Department of Pediatrics, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea. Jin Tack Kim Department of Pediatrics, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea. 2015 10 18 2015 10 18 Respiratory virus infection is a major cause of asthma exacerbation. However, the underlying mechanisms of  this exacerbation  are unknown. Therefore,  to  determine  the mechanisms, we examined the effect of influenza infection in a murine model of asthma.Mice were divided into four groups: the phosphate-buffered saline (PBS), house dust mite (HDM), influenza, and HDM/influenza groups. The influenza group and the HDM/influenza group were infected with influenza A virus. We measured airway resistance (Penh value), examined the lung tissue for pathology, and analyzed the cells and cytokines in bronchoalveolar lavage fluid (BALF) by ELISA.At 50 mg/mL methacholine, the HDM/influenza group showed a significantly higher Penh value than the PBS, HDM, and influenza groups. The number of neutrophils in BALF was higher in the HDM/influenza group than in the HDM group. A significantly greater number of lymphocytes and macrophages were detected in the HDM/influenza group than in the HDM group. IFN-γ and IL-1β levels were higher in the HDM/influenza group than in the HDM group. IL-5 levels did not vary between the HDM and HDM/influenza groups, IL-10 was significantly lower in the HDM/influenza than in the HDM group. Chemokine (C-X-C motif) ligand 1 (CXCL1) and regulated upon activation, normal T cell expressed and secreted (RANTES) were higher in the HDM/influenza group than in the HDM group.In a murine model of asthma, influenza-induced airway inflammation appeared to becaused by simultaneous activation of neutrophilic and eosinophilic inflammation. https://ijaai.tums.ac.ir/index.php/ijaai/article/view/586 https://ijaai.tums.ac.ir/index.php/ijaai/article/download/586/521