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2017 Fiscal Year Final Research Report

The role of chemokine CCL1 in experimental pulmonary emphysema induced by smoking exposure.

Research Project

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Project/Area Number 15K19411
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Respiratory organ internal medicine
Research InstitutionYamagata University

Principal Investigator

KIMURA Tomomi  山形大学, 医学部, 医員 (50536935)

Research Collaborator Shibata Yoko  
Sato Masamichi  
Sato Kento  
Nemoto Takako  
Project Period (FY) 2016-04-01 – 2018-03-31
Keywords慢性閉塞性肺疾患 / 肺気腫 / CCL1
Outline of Final Research Achievements

Wild type mice 7 to 9 weeks old and SPC - CCL 1 Tg mice were exposed by cigarette smoking. After 1 week and 2 weeks, bronchoalveolar lavage (BAL) was performed, and total cell number and cell fraction were examined. In BAL fluid two weeks later, the total number of cells was significantly increased in the SPC-CCL1 Tg mice than in the wild type mice. The majority of the cellular fraction was alveolar macrophage. It was revealed that macrophages were more strongly induced by smoking exposure in SPC-CCL1 Tg mice. These results suggested that CCL1 might play a major role in the differentiation and induction of alveolar macrophages, which plays a central role in inflammatory response in the lung due to smoking exposure.

Free Research Field

呼吸器内科学

URL: 

Published: 2019-03-29  

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