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Modulating toll-like receptor 4 signaling pathway protects mice from experimental colitis
https://fmu.repo.nii.ac.jp/records/2001841
https://fmu.repo.nii.ac.jp/records/20018414e969c0f-3161-4f46-8eed-7e712ec49646
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
FksmJMedSci_59_p81.pdf (855.9 KB)
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| Item type | デフォルトアイテムタイプ（フル）fmu(1) | |||||||||||||||
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| 公開日 | 2014-03-20 | |||||||||||||||
| タイトル | ||||||||||||||||
| タイトル | Modulating toll-like receptor 4 signaling pathway protects mice from experimental colitis | |||||||||||||||
| 言語 | en | |||||||||||||||
| 作成者 |
Saito, Keietsu
× Saito, Keietsu
× Katakura, Kyoko
× Suzuki, Ryoma
× Suzuki, Toshimitsu
× Ohira, Hiromasa
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| 権利情報 | ||||||||||||||||
| 言語 | en | |||||||||||||||
| 権利情報 | © 2013 The Fukushima Society of Medical Science | |||||||||||||||
| 主題 | ||||||||||||||||
| 言語 | en | |||||||||||||||
| 主題Scheme | Other | |||||||||||||||
| 主題 | LPS tolerance | |||||||||||||||
| 主題 | ||||||||||||||||
| 言語 | en | |||||||||||||||
| 主題Scheme | Other | |||||||||||||||
| 主題 | Toll-like receptor 4 | |||||||||||||||
| 主題 | ||||||||||||||||
| 言語 | en | |||||||||||||||
| 主題Scheme | Other | |||||||||||||||
| 主題 | experimental colitis | |||||||||||||||
| 内容記述 | ||||||||||||||||
| 内容記述タイプ | Abstract | |||||||||||||||
| 内容記述 | 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. | |||||||||||||||
| 言語 | en | |||||||||||||||
| 出版者 | ||||||||||||||||
| 出版者 | The Fukushima Society of Medical Science | |||||||||||||||
| 言語 | en | |||||||||||||||
| 言語 | ||||||||||||||||
| 言語 | eng | |||||||||||||||
| 資源タイプ | ||||||||||||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||||||||||||
| 資源タイプ | journal article | |||||||||||||||
| 出版タイプ | ||||||||||||||||
| 出版タイプ | VoR | |||||||||||||||
| 出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||||||||||||
| 関連情報 | ||||||||||||||||
| 関連タイプ | isIdenticalTo | |||||||||||||||
| 識別子タイプ | DOI | |||||||||||||||
| 関連識別子 | https://doi.org/10.5387/fms.59.81 | |||||||||||||||
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| 識別子タイプ | PMID | |||||||||||||||
| 関連識別子 | 24500383 | |||||||||||||||
| 関連情報 | ||||||||||||||||
| 識別子タイプ | ICHUSHI | |||||||||||||||
| 関連識別子 | 2015033200 | |||||||||||||||
| 収録物識別子 | ||||||||||||||||
| 収録物識別子タイプ | PISSN | |||||||||||||||
| 収録物識別子 | 0016-2590 | |||||||||||||||
| 収録物識別子 | ||||||||||||||||
| 収録物識別子タイプ | EISSN | |||||||||||||||
| 収録物識別子 | 2185-4610 | |||||||||||||||
| 収録物識別子 | ||||||||||||||||
| 収録物識別子タイプ | NCID | |||||||||||||||
| 収録物識別子 | AA0065246X | |||||||||||||||
| 書誌情報 |
en : Fukushima Journal of Medical Science 巻 59, 号 2, p. 81-88, 発行日 2013 |
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