KLF2通过调节细胞因子参与溃疡性结肠炎炎症调控的机制研究

Abstract

OBJECTIVE: Ulcerative colitis (UC) is a kind of chronic inflammatory bowel diseases that seriously endangers human health. The pathogenesis of UC is closely related to the intestinal immune response. Cytokines exert a key role in the regulation of intestinal inflammatory and immune responses. Abnormalities in the function and quantity of various cytokines or imbalance of inflammatory factors and immune factors would lead to UC development. We aimed to investigate whether Kruppel-like transcription factor 2 (KFL2) participates in the development of ulcerative colitis by regulating inflammation, so as to provide a new direction for the clinical treatment.PATIENTS AND METHODS: 40 UC patients were enrolled in this study, including 20 patients with mild ulcerative colitis (MUC) and 20 with severe ulcerative colitis (SUC). 20 normal end of intestinal tissues surgically resected from patients with colorectal cancer in the same period were selected as the control group. Hematoxylin-eosin (HE) staining was used to detect the inflammatory infiltration of intestinal mucosa tissues. Expressions of interleukin-6 (IL-6), interleukin-8 (IL-8), interleukin-10 (IL-10) and tumor necrosis factor-alpha (TNF-α) in peripheral blood mononuclear cells (PBMCs) of each group were detected by qRT-PCR (quantitative Real-Time Polymerase Chain Reaction). Immunohistochemistry was performed to observe the infiltration of IL-6 and TNF-α in intestinal mucosal tissues. Protein and mRNA levels of KLF2 in PBMCs of each group were detected by Western blot and qRT-PCR, respectively. The relationship between the mRNA level of KLF2 in PBMCs and expressions of IL-6, IL-8, IL-10, TNF-α were analyzed using qRT-PCR.RESULTS: Inflammatory cells and cytokines were infiltrated in the intestinal mucosa of UC patients. IL-6, IL-8, IL-10, and TNF-α were overexpressed in PBMCs of UC patients than those of controls. Protein and mRNA levels of KLF2 in PBMCs of UC patients were remarkably lower than those of controls, w