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Vol.59 (2013)  >

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Title: Modulating toll-like receptor 4 signaling pathway protects mice from experimental colitis
Authors: Saito, Keietsu
Katakura, Kyoko
Suzuki, Ryoma
Suzuki, Toshimitsu
Ohira, Hiromasa
Affiliation: 消化器・リウマチ膠原病内科学講座
Source title: Fukushima Journal of Medical Science
Volume: 59
Issue: 2
Start page: 81
End page: 88
Issue Date: 2013
Abstract: 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.
Publisher: The Fukushima Society of Medical Science
Publisher (Alternative foam): 福島医学会
language: eng
URI: http://ir.fmu.ac.jp/dspace/handle/123456789/372
Full text URL: http://ir.fmu.ac.jp/dspace/bitstream/123456789/372/1/FksmJMedSci_59_p81.pdf
ISSN: 0016-2590
DOI: 10.5387/fms.59.81
PubMed ID: 24500383
Related Page: http://dx.doi.org/10.5387/fms.59.81
Rights: © 2013 The Fukushima Society of Medical Science
Appears in Collections:Vol.59 (2013)

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