肠易激综合征腹泻型患者结肠黏膜Toll样受体2和4的表达

目的:研究Toll样受体(TLR)2、TLR4在肠易激综合征(IBS)患者和正常人结肠黏膜的表达.方法:研究30例IBS腹泻型患者及12名健康志愿者结肠黏膜TLR2和TLR4的表达,半定量分析TLR2及TLR4平均吸光度值.结果:与健康对照者相比,IBS患者结肠黏膜固有层水肿疏松.有大量的炎性细胞浸润.健康对照组和IBS组肠腔肠上皮细胞(IEC)的TLR2表达差异无统计学意义,(P<0.05).IBS患者的隐窝IEC的TLR2弱表达者较健康对照组少(6.7%比50.0%),而均匀表达增强者多(40.0%比0,P<0.05).86.7%的IBS患者基底侧及肠腔侧IEC均表达TLR4,较健康对照组增高(50.0%,P<0.05).细胞计数表明,IBS患者固有层TLR4阳性细胞数大于健康对照组(70.084±21.887比20.577±4.546,P<0.01),IBS患者的结肠黏膜TLR2及TLR4的吸光度值均增高单位分别为0.3079±0.0283比0.3886±0.0510和0.3044±0.0481比0.3971±0 0996(P<0 01).结论:IBS患者结肠有炎症表现,TLR2、TLR4存IBS发病中可能起一定作用.

Expressions of colonic Toll-like receptor 2/4 in patients with diarrhea predominant irritable bowel syndrome

Objective To study the expressions of Toll-like receptor (TLR)2 and TLR4 in colonic mucosa of patients with irritable bowel syndrome (IBS) and in normal subjects. Methods Thirty patients with diarrhea predominant IBS and 12 healthy volunteers were enrolled. The expressions of TLR2 and TLR4 in colonic mucosa were examined by immunohistochemistry (IHC).TLR2 and TLR4 were semi-quantitative analyzed with average absorbence. Results Contrast to healthy controls, the lamina propria of IBS patients showed edema and looseness with lots of inflammatory cells infiltration. There was no difference in expression of TLR2 between healthy controls and IBS patients (P>0.05). Compared with healthy controls, TLR2 in crypt epithelium and TLR4 in luminal surface of IBS patients were significantly up-regulated (TLR2 : 6.7 % vs. 50.0 %,TLR4: 40.0% vs. 0, P<0. 05). The TLR4 expressed in intestine epithelial cell of both the apical surface and the basolateral surface in 86.7% of patients with IBS, and in 50% of healthy controls.The positive cells of TLR4 in lamina propria were higher in patients with IBS than those in healthy controls (70. 084 ± 21. 887 vs. 20. 577 ± 4. 546, P<0.01). The A values of TLR2 and TLR4 in colonic mucosa of the patients with IBS were higher than those in healthy controls (TLR2:0. 3079±0. 0283vs. 0.3886±0. 0510,TLR4:0. 3044±0. 0481 vs. 0. 3971 ±:010996,P<0. 01). Conclusions Inflammatory cells infiltrated into colonic mueosa in patients with IBS suggested that inflammation might participate in the pathogenesis of IBS. Up-regulated expressions of TLR2 and TLR4 in IBS patients supposed that they might contribute to the occurrence of IBS.