Differential expression of occludin in patients with ulcerative colitis and healthy controls

Abstract

To the Editor: The etiology of inflammatory bowel disease (IBD) remains unknown. However, it has been postulated that IBD patients have a disruption of the intestinal barrier integrity that facilitates the trigger of an intestinal pathological process after exposure to several exogenous antigens. Barrier function is highly regulated, allowing the epithelium to control transmucosal permeability to solutes, water, and electrolytes. Occludin (OCLN) has a large cytoplasmic extension that may coordinate with the tight junctional complex, comprising a large number of membrane-associated proteins. OCLN is the first integral tight junction protein and the most ubiquitously expressed at the apical-most membranes. In order to confirm the contribution of OCLN gene in the pathogenesis of ulcerative colitis (UC), this is the first study to our best knowledge that explores the OCLN gene expression in colonic mucosa from patients with UC. We measured the OCLN gene expression from colonic biopsies of UC patients from September 2010 to July 2011. We studied a total of 54 individuals divided into three groups: 1) active UC (n 1⁄4 20); 2) remission UC (n 1⁄4 16); and 3) a healthy control group (n 1⁄4 18). Expression of mRNA OCLN was measured with the realtime polymerase chain reaction (RTPCR) method. The following primers were used: OCLN forward ggatgagc aatgccctttag and reverse aggaaccgaga gccaggt; and GADPH: forward gcccaa tacgaccaaatcc and reverse agccacatcgct cagaca for normalization. The OCLN mRNA expression was significantly decreased from colonic mucosa in UC remission patients as compared with the healthy control group (P 1⁄4 0.0001). Differential levels of expression were found between active and remission UC groups in OCLN gene expression, where active UC had significantly increased levels of OCLN compared to UC in remission (P 1⁄4 0.026), as shown in Figure 1. Our findings confirmed the potential role of OCLN in the pathogenesis of UC. This differential expression of OCLN between active and remission UC patients could be explained by the maintenance of epithelial cell polarity of the tight junction during the inflammatory process. Other proteins involved in the tight junction, like claudin-1 and claudin-2, were increased in patients with active IBD. In conclusion, expression of OCLN was elevated in colonic mucosa from the active UC compared to UC in remission and healthy control groups. Jesus K. Yamamoto-Furusho, MD, PhD, MSc Edgar J. Mendivil-Rangel, BS Gabriela Fonseca-Camarillo, PhD Inflammatory Bowel Disease Clinic Department of Gastroenterology Instituto Nacional de Ciencias Medicas y Nutricion Salvador Zubiran, Mexico