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福島県立医科大学学術成果リポジトリ = Fukushima Medical University Repository >
福島医学会 = The Fukushima Society of Medical Science >
Fukushima Journal of Medical Science >
Vol.59 (2013) >
このアイテムの引用には次の識別子を使用してください:
http://ir.fmu.ac.jp/dspace/handle/123456789/372
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| タイトル: | Modulating toll-like receptor 4 signaling pathway protects mice from experimental colitis |
| 著者: | Saito, Keietsu
Katakura, Kyoko
Suzuki, Ryoma
Suzuki, Toshimitsu
Ohira, Hiromasa |
| 学内所属: | 消化器・リウマチ膠原病内科学講座
病理学第二講座 |
| 誌名/書名: | Fukushima Journal of Medical Science |
| 巻: | 59 |
| 号: | 2 |
| 開始ページ: | 81 |
| 終了ページ: | 88 |
| 発行日: | 2013年 |
| 抄録: | Background/Aim: Several reports have indicated that environmental factors and defects in innate immunity are central to the pathogenesis of inflammatory bowel disease (IBD). Although bacteria producing lipopolysaccharide (LPS), which is a Toll-like receptor (TLR) 4 agonist, play a crucial role in the development of experimental colitis, LPS tolerance following initial exposure to LPS can result in a state of hyporesponsiveness to subsequent LPS challenge. Therefore, we initiated this study to explore the role of LPS tolerance in the development of colitis. Methods: Dextran sulfate sodium (DSS) colitis was induced in Balb/c mice with or without daily intraperitoneal administration of LPS. Disease activity and cytokine mRNA expression in the colon were evaluated. To confirm LPS tolerance, mouse conventional bone marrow-derived dendritic cells (BMDC) were preincubated with or without LPS, and were restimulated with LPS 24 h after first exposure. Cytokine production was measured by ELISA, and mRNA expression was evaluated by RT-PCR. Furthermore, we investigated the expression of negative regulators of LPS tolerance in BMDC. Results: Administration of LPS significantly suppressed colonic inflammation of DSS-induced colitis. After subsequent stimulation with LPS, TNF-α production was reduced in BMDC. IRAK-M, a negative regulator of TLR4 signaling, mRNA expression was up-regulated in LPS-treated BMDC. Conclusion: LPS tolerance was able to protect mice from DSS-induced colitis, and IRAK-M participated in this tolerance. Taken together, these observations suggest that loss of exposure to LPS is involved in the pathogenesis of IBD. |
| 出版者: | The Fukushima Society of Medical Science |
| 出版者（異表記）: | 福島医学会 |
| 本文の言語: | eng |
| このページのURI: | http://ir.fmu.ac.jp/dspace/handle/123456789/372 |
| 本文URL: | http://ir.fmu.ac.jp/dspace/bitstream/123456789/372/1/FksmJMedSci_59_p81.pdf |
| ISSN: | 0016-2590
2185-4610 |
| DOI: | 10.5387/fms.59.81 |
| PubMed番号: | 24500383 |
| 関連ページ: | http://dx.doi.org/10.5387/fms.59.81 |
| 権利情報: | © 2013 The Fukushima Society of Medical Science |
| 出現コレクション: | Vol.59 (2013)
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