P533 Relation between TL1A expression in intestinal mucosa, and endoscopic severity and clinical course in ulcerative colitis
Shimodaira, Y.(1)*;Yoshida, T.(1);Watanabe, K.(1);Takahashi, S.(1);Fukuda, S.(1);Koizumi, S.(1);Matsuhashi, T.(1);Iijima, K.(1);
(1)Akita University Graduate School of Medicine, Department of Gastroenterology and Neurology, Akita City, Japan;
TL1A is a TNF super family member cytokine encoded by TNFSF15 and reported to be a disease susceptibility gene for IBD. The relationship between TL1A expression and IBD pathophysiology, clinical course, endoscopic findings was not sufficiently clear. The aim of this study was to clarify the correlation between TL1A expression in the intestinal mucosa of UC and endoscopic severity, clinical severity, and clinical course.
The subjects were patients with UC who were visiting our hospital. Mucosal samples were biopsied from rectum with lower gastrointestinal endoscopy, and TL1A gene expression was examined by RT-PCR. We analyzed the relationship between patients’ background, clinical symptoms, blood test findings, and mucosal activity and TL1A expression.
A total of 77 specimens obtained with individual colonoscopy from 61 cases were included. Median age was 43, 36 cases were males, duration of disease was 2 years, the number of pancolitis was 54, median partial mayo score (pMayo) was 3, and the level of CRP was 1.5 mg/L. The number with Mayo endoscopic subscore (MES) of 0, 1, 2, and 3 were 14, 27, 24, and 12, respectively, and the mean TL1A expression was 1.76-, 1.09-, and 1.17-times higher in MES 1, 2, and 3 than in MES 0, respectively. TL1A expression was significantly higher in MES 1 than in MES 0 and MES 2. TL1A expression was significantly lower in the active group (pMayo 4 or higher) compared to the clinically low disease activity group (pMayo 3 or lower). TL1A expression was significantly lower with CRP ≥0.03 compared to CRP <0.03. TL1A expression was significantly higher in those with MES 1 at the initial onset than in those with MES 2 and 3. Eight cases were compared before and after induction therapy, and TL1A expression increased 1.9-fold after induction therapy. No correlation was found between the use of biologics and small molecular compounds and the expression of TL1A.
Relatively low activity in UC revealed higher mucosal expression of TL1A. TL1A is known to be secreted from various cell types such as macrophages and lymphocytes. It was suggested that the source of cell types and the amount of expression would alter according to the degree of inflammation.