The anti-inflammatory pathway regulated via nicotinic acetylcholine receptors in rat intestinal mesothelial cells

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Author(s)

    • MIHARA Taiki
    • Department of Veterinary Pharmacology, Graduate School of Agriculture and Life Sciences, The University of Tokyo, Bunkyo-ku, Tokyo 113-8657, Japan
    • OTSUBO Wataru
    • Department of Veterinary Pharmacology, Graduate School of Agriculture and Life Sciences, The University of Tokyo, Bunkyo-ku, Tokyo 113-8657, Japan
    • HORIGUCHI Kazuhide
    • Division of Anatomy, Department of Morphological and Physiological Sciences, University of Fukui Faculty of Medical Sciences, Fukui 910-1193, Japan
    • MIKAWA Shoma
    • Department of Veterinary Pharmacology, Graduate School of Agriculture and Life Sciences, The University of Tokyo, Bunkyo-ku, Tokyo 113-8657, Japan
    • KAJI Noriyuki
    • Department of Veterinary Pharmacology, Graduate School of Agriculture and Life Sciences, The University of Tokyo, Bunkyo-ku, Tokyo 113-8657, Japan
    • IINO Satoshi
    • Division of Anatomy, Department of Morphological and Physiological Sciences, University of Fukui Faculty of Medical Sciences, Fukui 910-1193, Japan
    • OZAKI Hiroshi
    • Department of Veterinary Pharmacology, Graduate School of Agriculture and Life Sciences, The University of Tokyo, Bunkyo-ku, Tokyo 113-8657, Japan
    • HORI Masatoshi
    • Department of Veterinary Pharmacology, Graduate School of Agriculture and Life Sciences, The University of Tokyo, Bunkyo-ku, Tokyo 113-8657, Japan

Abstract

<p>Regulation of inflammation in intestinal mesothelial cells in the abdominal cavity is important for the pathogeny of clinical conditions, such as postoperative ileus, peritonitis and encapsulating peritoneal sclerosis. Here we have examined the inflammatory effect of lipopolysaccharide (LPS) and the anti-inflammatory effect of nicotinic acetylcholine receptor stimulation in rat intestinal mesothelial cells. LPS upregulated mRNA expression of interleukin-1β (<i>IL-1β</i>), tumor necrosis factor-α (<i>TNF-α</i>), monocyte chemotactic protein-1 (<i>MCP-1</i>) and inducible nitric oxide synthase (<i>iNOS</i>). The α7, α9 and α10 subunits of nicotinic acetylcholine receptor were detected in intestinal mesothelial cells. Nicotine (10 nM) significantly inhibited LPS-induced mRNA expression of <i>IL-1β</i> and <i>iNOS</i>, but not <i>TNF-α and MCP-1</i>. In addition, the α7 nicotinic acetylcholine receptor selective agonist, PNU-282987 (10 nM), significantly inhibited LPS-induced mRNA expression of <i>IL-1β</i> but not <i>TNF-α, iNOS</i> and <i>MCP-1</i>. Finally, we found that enteric nerves adhered to intestinal mesothelial cells located under the ileal serosa. In conclusion, intestinal mesothelial cells react to LPS to induce the production of nitric oxide from <i>iNOS</i>. The anti-inflammatory action of intestinal mesothelial cells expressing α7nAChR may be mediated via their connectivity with enteric nerves.</p>

Journal

  • Journal of Veterinary Medical Science

    Journal of Veterinary Medical Science 79(11), 1795-1802, 2017

    JAPANESE SOCIETY OF VETERINARY SCIENCE

Codes

  • NII Article ID (NAID)
    130006199240
  • Text Lang
    ENG
  • ISSN
    0916-7250
  • Data Source
    J-STAGE 
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