The role of phospholipase Cepsilon in airway inflammation
Project/Area Number |
26860607
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Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Multi-year Fund |
Research Field |
Respiratory organ internal medicine
|
Research Institution | Kobe University |
Principal Investigator |
Nagano Tatsuya 神戸大学, 医学(系)研究科(研究院), 特命助教 (80624684)
|
Project Period (FY) |
2014-04-01 – 2016-03-31
|
Project Status |
Completed (Fiscal Year 2015)
|
Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
Keywords | PLCε / 肺線維症 / 国際情報交換 |
Outline of Final Research Achievements |
Phospholipase Cε(PLCε) is an effector of Ras and Rap small GTPases and is highly expressed in non-immune cells. PLCε has been shown to play a role in the development of T helper type 2 (TH2) cell-mediated airway inflammation. This study aimed to elucidate its role in the lung fibrosis by employing a bleomycin-induced pulmonary fibrosis model using the mutant mice where PLCε is enzymatically inactive. Pathohistological studies of the sections of the lung showed that infiltration of leukocytes and collagen deposition were greatly suppressed in PLCε deficient mice. The infiltration of neutrophils and lyphocytes in bronchoalveolar lavage fluid was suppressed in PLCε deficient mice. These results demonstrate an important role of PLCε in the lung fibrosis that mediated by neutrophils and lymphocyte.
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Report
(3 results)
Research Products
(1 results)