2016 Fiscal Year Annual Research Report
Analysis of the mechanism responsible for the onset of ulcerative colitis using S100 transgenic rats
Project/Area Number |
26460663
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Research Institution | Tenri Health Care University |
Principal Investigator |
池本 正生 天理医療大学, 医療学部, 教授 (80144385)
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Co-Investigator(Kenkyū-buntansha) |
戸田 好信 天理医療大学, 医療学部, 教授 (10444465)
竹田 真由 天理医療大学, 医療学部, 助教 (00423054) [Withdrawn]
仲瀬 裕志 京都大学, 医学研究科, 講師 (60362498)
岡田 光貴 天理医療大学, 医療学部, 助手 (80747569)
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Project Period (FY) |
2014-04-01 – 2017-03-31
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Keywords | トランスジェニックラット / マクロファージ / S100タンパク質 / 潰瘍性大腸炎 / 炎症性腸疾患 |
Outline of Annual Research Achievements |
The innate properties of S100A8 as a regulator in acute inflammation have not yet been elucidated in detail. Our aims are to newly establish S100A8 transgenic rats (Tg-S100A8) and clarify the immunological functions of S100A8. PCR and real-time PCR were performed to measure total mRNAs. S100A8 and S100A9 were detected in the large colon tissues of Tg-S100A8 and Wistar rats (WT) using Western blotting. The dynamic mobilities of the two proteins in macrophages were microscopically observed using fluorescent immunological staining. S100A8 mRNA was strongly expressed in several organ tissues of Tg-S100A8, such as the heart, stomach, small intestine, and macrophages. Following a treatment with 5% DSS for one week, decreases in body weights were significantly less in Tg-S100A8 than in WT. CRP serum levels were significantly lower in Tg-S100A8 than in WT. The dominant expression of S100A9 was detected in many macrophages in the rectal tissue of WT. IL-6 serum levels and the expression of mRNAs for IL-6 and TNF-alpha; were negatively regulated in the large colon of Tg-S100A8. An important result of the present study was that the expression of S100A8 mRNA was strongly induced in macrophages in Tg-S100A8, whereas that of mRNAs for some of the inflammatory cytokines described above was significantly reduced. Tg-S100A8 has potential as a useful experimental model rat not only for investigating the innate properties of S100A8 as a regulator, but also for clarifying its functional role in immune cells from a myeloid origin, particularly macrophages.
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