Chronic inflammation and molecular mechanism: atypical pneumonia and COPD

2014 Fiscal Year Final Research Report

• Project/Area Number: 23591481
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Infectious disease medicine
• Research Institution: Juntendo University (2014); Kyorin University (2011-2013)
• Principal Investigator: WADA HIROO 順天堂大学, 医学(系)研究科(研究院), 准教授 (50407053)
• Co-Investigator(Renkei-kenkyūsha): GOTO Hajime 杏林大学, 医学部, 教授 (80134617)
• Project Period (FY): 2011-04-28 – 2015-03-31
• Keywords: IL-10 / IL-17 / マウスモデル / マイコプラズマ / 感染症

Outline of Final Research Achievements

Because it is observed that Mycoplasma pneumonia (Mp) pneumonia exacerbates COPD, both Mp pneumonia and COPD may share common molecular pathogenesis. In order to the common pathogenesis, mice were exposed to either Mp compoents or to cigarette smoke, and then analyzed.
Immunihistochemical analyses on mice exposed to Mp pneumonia revealed that pulmonary migration of neutrophil increased which increasingly expressed IL-23 protein. Mice deficient with IL-10 gene showed that pulmonary chemotaxis and MMP-9 expression in the lung were enhanced, compared to the wild type controls. Both data suggested that IL-17 was involved in the pathogenesis. Since IL-17 has at least 6 subtypes, and its detection is rather difficult, further analyses, probably using IL-17 deficient mice, are essential.

Free Research Field

呼吸器内科学