2017 Fiscal Year Final Research Report
The role of chemokine CCL1 in experimental pulmonary emphysema induced by smoking exposure.
Project/Area Number |
15K19411
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Respiratory organ internal medicine
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Research Institution | Yamagata University |
Principal Investigator |
|
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.
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Free Research Field |
呼吸器内科学
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