VIP in Inflammatory Bowel Disease: State of the Art
Catalina Abad, Rosa Gomariz, James Waschek, Javier Leceta, Carmen Martinez, Yasmina Juarranz and Alicia Arranz
Affiliation: The Semel Institute and Department of Psychiatry, The David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA.
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.
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.
Rights & PermissionsPrintExport