Background: Osteopontin (OPN) is associated with the Th1 immune response in inflammatory bowel diseases (IBD). While OPN has been shown to play an important role in maintaining the epithelial barrier, its role in IBD remains unclear.
Aim: The aim of this study was to assess OPN function in patients with IBD and in the mouse colitis model.
Methods: Osteopontin expression in colonic samples from IBD patients was determined by a semi-quantitative immunohistochemical staining method. Colitis in BALB/c mice was induced by 5 % dextran sodium sulfate (DSS), followed by treatment with salazosulfapyridine (SASP) and infliximab, respectively. The plasma OPN concentration was measured by an enzyme-linked immunosorbent assay. The expression of OPN in colonic tissues was detected by reverse transcriptase PCR, real-time PCR and Western blot, and the localization of OPN was determined by a semi-quantitative immunohistochemical staining method. The immune function of OPN was investigated by measuring the production of cytokines, and the amount of cytokines produced was then used to determine OPN immune functions.
Results: Osteopontin expression in intestinal epithelial cells was significantly lower in IBD patients than in controls, while its expression in lamina propria exudative cells was significantly higher in IBD patients than in controls. In DSS-induced mice, OPN expression in plasma and colonic tissues increased significantly, and this increase was significantly reduced after the mice were treated with SASP and infliximab. OPN promoted the Th1 immune response and strengthened inflammation in the mouse colitis model.
Conclusions: Our results indicate that OPN plays an important role in the immune response and is also involved in the mucosal protective mechanism in IBD.