KFL2 participates in the development of ulcerative colitis through inhibiting inflammation via regulating cytokines.

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, which were more significant in SUC patients. Meanwhile, KLF2 was closely related to expressions of IL-6, IL-8, IL-10, and TNF-α in PBMCs of UC patients.

CONCLUSIONS

KLF2 was downregulated in PBMCs of UC patients than that of normal controls, which participated in the inflammatory response of UC by regulating expressions of IL-6, IL-8, IL-10, and TNF-α. KLF2 may suggest new treatments for ulcerative colitis.