Mechanism of asthma exacerbations induced by rhinovirus and RS virus infection and its genome array analysis

2014 Fiscal Year Final Research Report

• Project/Area Number: 24591565
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Pediatrics
• Research Institution: Tokai University (2014); Gunma Institute of Public Health and Environmental Sciences (2012-2013)
• Principal Investigator: KATO Masahiko 東海大学, 医学部, 准教授 (30292593)
• Co-Investigator(Kenkyū-buntansha): YAMADA Yoshiyuki 群馬県衛生環境研究所, 研究企画係, 研究員 (80309252) ; HAYASHI Yasuhide 群馬県衛生環境研究所, 研究企画係, 研究員 (30238133)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: ウイルス感染 / 好酸球 / 気管支喘息 / サイトカイン

Outline of Final Research Achievements

We investigated the effects of eosinophil granule proteins on bronchial epithelial cell infected with RS virus. Morphological changes in human type II pulmonary alveolar epithelial cells, A549 with RS virus and/or eosinophil granule proteins such as MBP, EPO, ECP, and EDN were observed by microscopy. Apoptosis/necrosis was evaluated by trypan blue exclusion test. We also measured 27 types of cytokines/chemokines production in supernatant of the cells and 12 types of phosphorylated proteins in the cells. MBP or EPO induced cytotoxicity and necrosis of A549 cells with RS virus. GM-CSF and IL-17 production was elevated in RS virus- and MBP-treated A549 cells. MBP induced the phosphorylation of ERK 1/2, p38 MAPK, JNK, and STAT 3 in A549 cells with RS virus. Eosinophil granule proteins specifically MBP damage RS virus-infected bronchial epithelial cells, indicating that eosinophilic inflammation might be associated with pathophysiology of RS virus-induced acute exacerbations of asthma.

Free Research Field

小児アレルギー学