| Project/Area Number |
25461155
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Kyoto University |
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Principal Investigator |
Matsumoto Hisako 京都大学, 医学(系)研究科(研究院), 助教 (60359809)
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| Co-Investigator(Kenkyū-buntansha) |
MURO SHIGEO 京都大学, 医学研究科, 講師 (60344454)
SATO ATSUYASU 京都大学, 医学研究科, 特定病院助教 (30706677)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥390,000 (Direct Cost: ¥300,000、Indirect Cost: ¥90,000)
Fiscal Year 2014: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 喫煙喘息 / ADAM33 / エピゲノム解析 / 喫煙暴露 / 気道平滑筋細胞 |
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| Outline of Final Research Achievements |
Here we aimed to clarify genomic/epigenomic changes in smoking-associated airway inflammation, which is characterized with mixed type inflammation of eosinophilic/type 2 and neutrophilic inflammations in asthma. In clinical samples, we found that sensitization to staphylococcus aureus enterotoxins (SE) was associated with smoking status. However, stimulation with SE to cultured airway smooth muscle cells did not show any significant changes in several cytokines that were candidate for epigenomic analysis. We then focused on genotyping of eosinophilic/type 2 asthmatics, which lead to identification of SNPs of IL4Rα and ADAM33 as important genome markers of asthma exacerbations. More importantly, a SNP of ADAM33 was associated with mixed type inflammation, which is a typical endotype of smoker asthma. These findings may be a clue to understand smoking-associated airway inflammation and efficient analysis of the epigenetic changes, which is closely associated with genomic changes.
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