P087 Calcitonin gene related peptide beta (CGRPβ): a new player in inflammatory bowel disease pathophysiology

Abstract

Abstract Background Calcitonin gene related peptide (CGRP) is mainly present in the central nervous system (α isoform) and enteric nervous system (β isoform). CGRP is known to be the most potent vasodilator of the body, and it promotes migration of inflammatory cells. Although its function in the gut is not well established yet, CGRPβ is postulated to have a protective role against inflammation in the gut, promoting migration of inflammatory cells, regulating nociception, motility and gut microbioma. The aim of the study is to analyse serum levels of CGRPβ in patients newly diagnosed with inflammatory bowel disease (IBD), to unravel its potential role in the disease. Methods CGRPβ levels were measured by ELISA (CUSABIO, China) in early morning samples of newly diagnosed patients with IBD. Classification of the disease (ulcerative colitis- UC, Crohn’s disease- CD or unclassified inflammatory bowel disease- U-IBD), demographic data and treatment during sample collection were also collected. The results were compared with healthy controls (HC) stratified by age and sex. Statistical analysis was performed using SPSS and CGRPβ levels were compared with Mann-Whitney and Dunn’s tests. Results Seventy-one patients with newly diagnosed IBD (mean age 48.3±16.5 years, 63.4% females) were matched with 71 HC (mean age= 48.2±16.7 years-64.8% females). Samples were collected between 0 and 249 days after IBD diagnosis was established (median 49 days, interquartile range 29-66 days). Thirty patients were diagnosed as CD, 36 as UC and 5 as U-IBD. Most patients with CD had ileal location and inflammatory behaviour. One of these patients was on methotrexate due to a prior diagnosis of rheumatoid arthritis; the rest were either with no treatment, aminosalicylates, steroids or budesonide, or some combination of these. Half of the patients with UC had proctitis. Six had no treatment, and the rest were prescribed aminosalicylates, seven of them in combination with steroids. These characteristics are shown in table 1. Serum CGRPβ levels in patients with IBD were significantly decreased (2.95±1.68 pg/mL) compared to HC (4.65±2.59 pg/mL), (p<0.0001). These results stayed significant, in both CD (3.15±2.08 pg/mL; p<0.05), and UC (2.83±12.7 pg/mL; p <0.01), but not in IBD-U (2.56±1.73 pg/mL), though the number of U-IBD cases was low. CGRPβ concentrations did not differ significantly in patients with CD and UC. The results are illustrated in figures 1 and 2. Conclusion The consistent decrease in CGRPβ levels in IBD shown here strongly supports a protective role of this peptide in the homeostasis of the intestinal mucosa. This work was supported by a grant from the Instituto de Salud Carlos III (PI20/01358).