Investigation of the relationship between the Th17/IL-23 pathway and innate-adaptive immune system in TNBS-induced colitis in rats

Abstract

<strong><em>Objective(s)</em></strong>: This study was aimed at investigating immune activations of the 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis model in colonic mucosa by immunohistochemical and Western blot methods.<br /> <strong><em>Materials and Methods: </em></strong>For this purpose, 16 female Wistar albino rats were divided into two random groups of control (n=8) and colitis (n=8). The experimental colitis model was induced by intracolonic administration of TNBS (25 mg/rat). Control animals received only rectal saline for the same time. The animals were sacrificed on the 15^th day after TNBS administration, and colon tissue was removed and examined morphologically. Colon samples were stained immunohistochemically with anti-CD3, anti-CD4, anti-CD5, anti-CD8, anti-CD11b, anti-CD45, anti-TNF-α, anti-IL-17, anti-IL-22 and anti-IL-23 antibodies. Additionally, the colonic tissue IL-17 and IL-22 expressions were examined by the Western blot method.<br /> <strong><em>Results:</em></strong> In the experimental results, it was determined that there was a significant decrease in body weight and an increase in colon weight in the colitis group when comparing initial experiments. The colon tissue ulcerations, inflammation, crypt loss and Goblet cell loss were observed in the colitis group in microscopic examinations. The immunohistochemical positive cell numbers significantly increased in the colitis group. The immunoreactive lymphocytes in the propria, intracryptal and submucosal layers were found to be increased in the colitis group of rats. In addition, IL-17 and IL-23 expressions were increased in colitis colon mucosa found by Western blot analysis.<br /> <strong><em>Conclusion:</em></strong> The Th17/IL-23 pathway and IL-22 serve important roles in the pathogenesis of ulcerative colitis, and will be further examined by study.