Introduction: Alterations in TJ structure and function have been seen in both IBD and experimental models of inflammation. Studies have shown a decrease in key TJ proteins such as ZO-1 and occludin. Our group has also shown an increase in claudin-1, a transmembrane TJ protein, in DSS induced colitis. We hypothesize that claudin-1 is upregulated in intestinal inflammation. Methods: IEC-18 cells (ileal cell line) were treated with 0, 5, 50, or 100ng/ml of TNFα for 48 hours(n=4 all doses). Operative intestinal samples from patients with UC (colon), CD (terminal ileum (TI)), or a non-inflammatory condition (normal, both colon and TI) were collected and mucosa isolated. Western blots were performed on IEC-18 cells and tissue samples for claudin-1. Blots were stripped for actin as a loading control. UC and CD mucosal samples were compared to their respective controls with an unpaired t-test, IEC-18 samples were compared with ANOVA. Results: There was a significant increase in claudin-1 expression with 50 and 100ng/ml of TNFα (see fig). There was significantly more claudin-1 expression in UC compared to normal, p<0.0007 (see fig). Claudin-1 was increased in the TI of CD patients and approached statistical significance, p=0.05.Conclusions: 1. Treatment with TNFα, a key inflammatory cytokine in IBD, led to a significant increase in claudin-1 in IEC-18 cells. 2. There was a significant increase in claudin-1 in diseased colon in UC and an increase approaching statistical significance in diseased TI in CD. The increase in claudin-1 seen in inflammation may be a compensatory mechanism to maintain structural integrity of the TJ despite the loss of key proteins, ZO-1 and occludin.