Functional analysis of CCL1 on development and exacerbation of interstitial pneumonia by SPC-CCL1 transgenic mice.

2016 Fiscal Year Final Research Report

• Project/Area Number: 26461153
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Respiratory organ internal medicine
• Research Institution: Yamagata University
• Principal Investigator: INOUE Sumito 山形大学, 医学部, 助教 (70466621)
• Co-Investigator(Renkei-kenkyūsha): SHIBATA Yoko 山形大学, 医学部, 講師 (60333978) ; ABE Shuichi 山形大学, 医学部, 非常勤講師 (40400543)
• Research Collaborator: IGARASHI Akira 山形大学, 医学部, 助教 (40637170)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: 間質性肺炎 / ケモカイン / CCL-1

Outline of Final Research Achievements

CCL1 transgenic mice (SPC-CCL1 Tg mice), overexpressing CCL1 specifically in the lungs were newly produced and examined in a BCG infection model. As a result, there was an increase in granuloma and suppression of interstitial inflammation in the lung in these mice. DNA microarray analysis revealed increased expression in 47 genes associated with "response to biological stress", Ern1 involved in endoplasmic reticulum stress and granulomatous formation, immunoglobulin related genes such as Ighg, IGHV, Igk-V5 expressions enhancement were observed. Enhancement of expression of Phospho-Ire1, an autophosphorylated form of Ire1 which is an Ern-1 encoded endoplasmic reticulum transmembrane kinase, was observed.

Free Research Field

呼吸器内科