The pathogenesis of inflammatory bowel syndrome (IBD), which includes Crohn’s disease (CD) and ulcerative
colitis (UC) is poorly understood. However, an inflammatory component is a common hallmark. It has been suggested
that CD principally involves Th1 and/or Th17 cells, while UC is considered to be more Th2 driven. Because vasoactive
intestinal peptide (VIP) has emerged in the last decade as a putative candidate for the treatment of inflammatory diseases
with a Th1 component, it may as well serve as a therapeutic target in CD. In addition, experiments using mice deficient in
VIP or its receptors have revealed that the endogenously-produced VIP may participate in the regulation of immunity. The
aim of the present review is to summarize the quite considerable array of data which suggests that the VIP-receptor
system plays a key role in modulating multiple molecular and cellular players involved in IBD.
Keywords: Crohn’s disease, IBD, inflammation, neuroimmunomodulation, neuropeptide, VIP, Autoimmune diseases, ulcerative colitis (UC), predominant anti-inflammatory action, neuroimmunopeptide, pituitary adenylate cyclaseactivating polypeptide (PACAP), airflow obstruction, airway inflammation.
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