Ｃｌｏｓｔｒｉｄｉｕｍ　ｄｉｆｆｉｃｉｌｅ　ｔｏｘｉｎ　Ａ誘発腸炎におけるサイトカインの役割‐ＩＦＮ‐γの生物学的役割より‐

DOI 参考文献31件
  • 石田 裕子
    金沢大学がん研究所組織分子構築分野 和歌山県立医科大学法医学教室
  • 近藤 稔和
    和歌山県立医科大学法医学教室
  • 向田 直史
    金沢大学がん研究所組織分子構築分野

書誌事項

タイトル別名
  • The pathogenic roles of IFN-.GAMMA. in Clostridium difficile toxin A-induced enteritis
  • ―IFN-γの生物学的役割より―

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抄録

Clostridium difficile (C. difficile) is a major causative agent of antibiotics-associated diarrhea and pseudomembranous colitis in humans. Pathogenic strains of C. difficile release toxin A, which is referred as enterotoxin due to its capacity to disrupt intestinal epithelial structure. Toxin A causes tissue damages directly by glucosylation of Rho and indirectly by inducing massive infiltration of neutrophils. We previously observed that interferon (IFN)-γ-deficient mice exhibited less neutrophil infiltration and tissue damages in several types of acute inflammation in liver. These observations prompted us to explore the roles of IFN-γ in toxin A-induced acute enteritis model. Injection of toxin A into ileal loops caused massive fluid secretion, disruption of epithelial structure, and massive neutrophil infiltration in wild-type (WT) mice, accompanied with increases in IFN-γ mRNA expression and protein contents in the intestine. A double-color immunofluorescence analysis detected IFN-γ protein in infiltrating neutrophils and to a lesser degree, CD3-positive lymphocytes. On the contrary, toxin A failed to induce fluid secretion, disruption of intestinal epithelial structure, and neutrophil infiltration in IFN-γ-deficient mice. Similarly, pretreatment of neutralizing anti-IFN-γ antibody prevented toxin A-induced enteritis. These observations suggest that IFN-γ is a good molecular target for the control of C. difficile-associated pseudomembranous colitis.

収録刊行物

  • 炎症・再生

    炎症・再生 25 (6), 507-511, 2005

    一般社団法人 日本炎症・再生医学会

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