Tu1130 Simple Endoscopic Score for Crohn's Disease (SES-CD) Predicts Clinical Remission in Patients With Crohn's Disease

Abstract

Introduction: Centaurin Beta 1 (CENTB1) also named ACAP1, previously identified as a GTPase-activating protein, is a member of the ADP ribosylation factor family [1]. This protein is encoded by a gene located on the short arm of human chromosome 17. A previous study showed that CENTB1 binds to NOD1 and NOD2, and serves as a cytosolic down-regulator of NF-kB activation in response to γ-D-glutamyl-meso-diaminopimelic acid (iE-DAP) and muramyl dipeptide (MDP-LD) stimulation in intestinal epithelial cells. No previous have explore the expression of CENTB1 in patients with Ulcerative Colitis (UC). Aim: To study the CENTB1 gene and protein expression in patients with UC. Patients and Methods: We measured the CENTB1 gene expression from colonic biopsies from three groups: 1) Active UC (n=20); 2) Remission UC (n=20); and Healthy control group (n=20). All individuals were assessed for CENTB1 mRNA transcripts levels relative to GAPDH constitutive gene using Real Time Polymerase Chain Reaction using LNA TaqMan® probes from Roche in combination with target gene specific primers: CENTB1 left: atgccacccaacacacact and right: gaaaccccgcagaccttc; and GAPDH left: agccacatcgctcagaca and right: gcccaatacgaccaaatcc for normalization. The detection of CENTB1 protein in tissue was performed by immunohistochemistry. Results: The CENTB1 gene expression was significant up-regulated in colonic mucosa from patients with active UC compared to remission UC and the healthy control group (P= 0.006 and P=0.031 respectively). Also, a marginal increased gene expression of CENTB1 was detected in the UC remission group compared to the healthy control group (P=0.04). In order to confirm the localization of CENTB1 protein in colonic tissue (in situ), we performed a detailed immunohistochemical analysis for CENTB1 in inflamed and noninflamed colonic tissue from UC patients. The percentage of centaurin beta 1 producing cells was higher in UC patients compared with controls. Centaurin beta1+ cells were localized mainly in inflammatory infiltrates, predominantly polymorphonuclear cells, which extended from the adventitia to mucosa, being more abundant in epithelial cells (p=0.04) and adventitia. Conclusion: The CENTB1 was up-regulated in patients with active UC as compared to UC remission and healthy control groups suggesting that it is involved in the inflammatory process.