Expression and significance of mucosal β-defensin-2,TNFα and IL-1β in ulcerative colitis CHANG
- VernacularTitle:溃疡性结肠炎黏膜中β防御素2与肿瘤坏死因子α和白细胞介素1β的表达及相互关系
- Author:
Yuying CHANG
;
Qin OUYANG
- Publication Type:Journal Article
- Keywords:
Beta-defensins;
Colitis,ulcerative;
Tumor necrosis factor;
Interleukin-1
- From:
Chinese Journal of Internal Medicine
2008;47(1):11-14
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the expression and significance of human β-defensin-2 (HBD2),TNFα and IL-1βin ulcerative colitis(UC).Methods Thirty-five patients with active UC diagnosed by the department of gastroenterology in West China Hospital were included in this study.Ulcerative colitis disease activity index(UCAI)was assessed and the pathological grades of UC were classified.Immunohistochemistry assay and real-time quantitative PCR were used for the expression of HBD2,TNFα,IL-1β in colonic mucosa of UC.Results Among the 35 patients with UC,10 cases were mild.13 moderate and 12 severe.Of the 35 cases.there were 11 with grade Ⅰ.13 grade Ⅱ and 11 grade Ⅲ lesion according to Truelove criteria.The score of UCAI had positive correlation with pathological grading (r=0.890,P＜0.01).The expressions of HBD2,TNFα,IL-1β in colonic mucosa of UC with immunohistochemistry and real-time quantitative PCR were significantly higher than those in healthy control (P＜0.05);the expressions increased gradually with the severity of pathological grade and there was a higher expression of them in inflamed area than in non-inflamed(P＜0.05).A good positive correlation was also found between HBD2 and other inflammatory cytokines.Conclusions It is shown that there is a higher expression of HBD2 in colonic mucosa as compared with healthy control.a higher expression of it in inflamed area than in non-inflamed area and a positive correlation of expression between HBD2 and pro-inflammatory cytokines such as TNFα and IL-1 β,implying that HBD2 and pro-inflammatory cytokines are interdependent and interactive playing an important role in magnifying and aggravating inflammatory injury in UC.
