Role of Muscarinic Acetylcholine Receptors in Intestinal Epithelial Homeostasis: Insights for the Treatment of Inflammatory Bowel Disease

  • Junsuke Uwada
    Department of Pharmacology, School of Medicine, Kanazawa Medical University, Uchinada 920-0293, Japan
  • Hitomi Nakazawa
    Department of Pharmacology, School of Medicine, Kanazawa Medical University, Uchinada 920-0293, Japan
  • Ikunobu Muramatsu
    Department of Pharmacology, School of Medicine, Kanazawa Medical University, Uchinada 920-0293, Japan
  • Takayoshi Masuoka
    Department of Pharmacology, School of Medicine, Kanazawa Medical University, Uchinada 920-0293, Japan
  • Takashi Yazawa
    Department of Biochemistry, Asahikawa Medical University, Asahikawa 078-8510, Japan

Description

<jats:p>Inflammatory bowel disease (IBD), which includes Crohn’s disease and ulcerative colitis, is an intestinal disorder that causes prolonged inflammation of the gastrointestinal tract. Currently, the etiology of IBD is not fully understood and treatments are insufficient to completely cure the disease. In addition to absorbing essential nutrients, intestinal epithelial cells prevent the entry of foreign antigens (micro-organisms and undigested food) through mucus secretion and epithelial barrier formation. Disruption of the intestinal epithelial homeostasis exacerbates inflammation. Thus, the maintenance and reinforcement of epithelial function may have therapeutic benefits in the treatment of IBD. Muscarinic acetylcholine receptors (mAChRs) are G protein-coupled receptors for acetylcholine that are expressed in intestinal epithelial cells. Recent studies have revealed the role of mAChRs in the maintenance of intestinal epithelial homeostasis. The importance of non-neuronal acetylcholine in mAChR activation in epithelial cells has also been recognized. This review aimed to summarize recent advances in research on mAChRs for intestinal epithelial homeostasis and the involvement of non-neuronal acetylcholine systems, and highlight their potential as targets for IBD therapy.</jats:p>

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