Published online Jul 28, 2017. doi: 10.3748/wjg.v23.i28.5068
Peer-review started: February 16, 2017
First decision: April 5, 2017
Revised: April 13, 2017
Accepted: July 12, 2017
Article in press: July 12, 2017
Published online: July 28, 2017
Processing time: 164 Days and 4.4 Hours
Inflammatory bowel disease (IBD) is a chronic recurrent condition whose etiology is unknown, and it includes ulcerative colitis, Crohn’s disease, and microscopic colitis. These three diseases differ in clinical manifestations, courses, and prognoses. IBD reduces the patients’ quality of life and is an economic burden to both the patients and society. Interactions between the gastrointestinal (GI) neuroendocrine peptides/amines (NEPA) and the immune system are believed to play an important role in the pathophysiology of IBD. Moreover, the interaction between GI NEPA and intestinal microbiota appears to play also a pivotal role in the pathophysiology of IBD. This review summarizes the available data on GI NEPA in IBD, and speculates on their possible role in the pathophysiology and the potential use of this information when developing treatments. GI NEPA serotonin, the neuropeptide Y family, and substance P are proinflammatory, while the chromogranin/secretogranin family, vasoactive intestinal peptide, somatostatin, and ghrelin are anti-inflammatory. Several innate and adaptive immune cells express these NEPA and/or have receptors to them. The GI NEPA are affected in patients with IBD and in animal models of human IBD. The GI NEPA are potentially useful for the diagnosis and follow-up of the activity of IBD, and are candidate targets for treatments of this disease.
Core tip: Approximately 80% of the body immune cells (IC) are localized in the gastrointestinal (GI) tract close to the GI neuroendocrine regulatory system (NES). Many IC express GI neuroendocrine peptides/amines (NEPA) and possess receptors to several NEPA. Several GI NEPA are abnormal during active inflammatory bowel disease (IBD) in both patients and animal models of IBD. The changes in the GI NEPA are correlated with those of the IC during the inflammatory process. Studying the interactions between the GI NES and the immune system in IBD may improve our understanding of the pathophysiology of IBD and provide us with new tools for treatment.