Kim Hwan Soo, Lee Huisu, Kim Hyun Sook, Won Sulmui, Lee Eu Kyoung, Bang Kyongwon, Chun Yoon Hong, Yoon Jong-Seo, Kim Hyun Hee, Kim Jin Tack
Department of Pediatrics, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
Iran J Allergy Asthma Immunol. 2015 Aug;14(4):392-401.
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 be caused by simultaneous activation of neutrophilic and eosinophilic inflammation.
