Multiple targets of carbon monoxide gas in the intestinal inflammation.
Inflammatory bowel diseases (IBDs) such as ulcerative colitis and Crohn's disease are chronic relapsing and remitting inflammatory disorders of the intestinal tract. It is important to investigate the precise pathogenesis of IBD, to evaluate new anti-inflammatory agents, and to develop novel drugs. Carbon monoxide (CO) has emerged as an important regulator of acute and chronic inflammation of the gastrointestinal tract. The mechanism underlying its anti-inflammatory effects is only partially understood. Recent reports have demonstrated that CO could play a role in the functional modulation of epithelial and immunological cells in the intestine. In this short review, we have highlighted the recent findings that CO stimulates the epithelial cell restitution and FGF production from myofibroblasts. CO was also shown to regulate T cell activation and differentiation, and to activate macrophages. Finally, we have discussed the direction of translational research with respect to launching a novel agent for releasing CO in the intestine.
Molecular Gastroenterology and Hepatology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Kyoto, 602-8566, Japan. Electronic address: ynaito@koto.kpu-m.ac.jp.
Yuji
Y
Naito
Molecular Gastroenterology and Hepatology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Kyoto, 602-8566, Japan.
Tomohisa
T
Takagi
Molecular Gastroenterology and Hepatology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Kyoto, 602-8566, Japan.
Kazuhiko
K
Uchiyama
Molecular Gastroenterology and Hepatology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Kyoto, 602-8566, Japan.
Kazuhiro
K
Katada
Molecular Gastroenterology and Hepatology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Kyoto, 602-8566, Japan.
Toshikazu
T
Yoshikawa
D000818:Animals; D002248:Carbon Monoxide / Q000378:metabolism*; D002454:Cell Differentiation; D003092:Colitis / Q000378:metabolism* / Q000473:pathology; D016207:Cytokines / Q000378:metabolism; D006801:Humans; D007413:Intestinal Mucosa / Q000473:pathology; D008213:Lymphocyte Activation; D008214:Lymphocytes / Q000166:cytology*
D016207:Cytokines; D002248:Carbon Monoxide
CO-Releasing molecule; Carbon monoxide; Epithelial restitution; Inflammatory bowel disease; Macrophage activation; T cell differentiation