2018 Fiscal Year Final Research Report
Elucidation of the mechanism of asthma condition deterioration in the obese environment and the establish of treatment development
| Project/Area Number |
16H06224
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| Research Category |
Grant-in-Aid for Young Scientists (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
Pathological medical chemistry
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| Research Institution | Kazusa DNA Research Institute (2018)
Chiba University (2016-2017) |
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Principal Investigator |
Endo Yusuke 公益財団法人かずさDNA研究所, 先端研究開発部, 室長 (80612192)
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| Research Collaborator |
NAKAYAMA TOSHINORI
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Keywords | 肥満 / 喘息 / Tpath2 / ILC2 / ACC1 / 脂質代謝 |
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| Outline of Final Research Achievements |
This study focused on pathogenic Th2 (Tpath2) cells and group 2 innate cells (ILC2), and aimed to understand the mechanism of onset and chronicity of obesity-induced asthma. The following contents were clarified within the research period. 1. The aggravated asthmatic condition in obese environment was observed. 2. An increase in Tpath2 cells was observed in lung tissue in an obese environment. An increase was also detected for ILC3. 3. It was shown that not only endogenous fatty acid synthesis but also the uptake of fatty acid from the environment is important for the functional acquisition of Tpath2 and ILC2. 4. Obesity-induced asthma was improved by inhibiting lipid metabolism of Tpath2 or ILC2.
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| Free Research Field |
免疫学
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| Academic Significance and Societal Importance of the Research Achievements |
本研究の成果より、Tpath2やILC2など生体に有害となる細胞の特殊な「脂肪酸代謝」という観点から喘息の発症・慢性化メカニズムにアプローチすることで、脂肪酸もしくはその合成経路をターゲットとした治療法開発が可能となる。具体的には、ACC1や特定の脂肪酸代謝経路をターゲットとした創薬や脂肪酸自体の食習慣によって肥満誘導性喘息を改善する基盤の構築が可能となるのである。また、本研究の成果は、肥満誘導性の喘息治療に留まらず、他の慢性アレルギー疾患の誘導・慢性化メカニズムの解明・新規診断ツール・治療法の足がかりとなり、肥満誘導性の慢性炎症疾患の解明に大きく貢献できる。
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