Hp感染胃黏膜IL-17、TLR2及PD-1表达及意义

Expression and significance of IL - 17, TLR2 and PD - 1 in the gastric mucosa of patients with Hp infection

目的探讨幽门螺杆菌（Hp）阳性萎缩性胃炎中胃黏膜免疫损伤机制，为临床寻找根除Hp新的方法或靶点提供理论依据。方法收集胃镜下钳取40例浅表性胃炎（Hp阴性浅表性胃炎20例、Hp阳性浅表性胃炎20例），40例萎缩性胃炎（Hp阴性萎缩性胃炎20例、Hp阳性萎缩性胃炎20例）胃黏膜标本。采用免疫组织化学方法检测白细胞介素-17（IL-17）、T011样受体2（TLR2）及程序性死亡受体1（PD-1）表达。结果①Hp阳性浅表性胃炎胃黏膜中IL-17、PD-1表达量高于Hp阴性浅表性胃炎，Hp阳性萎缩性胃炎中IL-17、PD-1表达量高于Hp阴性萎缩性胃炎，差异有统计学意义（P〈0．05）。②Hp阳性萎缩性胃炎胃黏膜中IL-17、PD-1表达量高于Hp阳性浅表性胃炎，差异有统计学意义（P〈0．05）。③各组胃黏膜中TLR2均无表达。结论Hp感染可上调IL-17、PD-1的表达，Hp感染后疾病的进展与IL-17、PD-1高表达有关，说明IL-17、PD-1在抗Hp的同时具有造成免疫损伤作用。TLR2在Hp感染胃黏膜反应中不参与免疫反应或不参与机体对Hp感染引起免疫应答。

Objective To investigate the immunological mechanism of mucosa injury in patients with Helicobacter pylori （Hp） positive atrophic gastritis and provided theoretical evidence for new method or targets to eradicate Hp. Methods Mucosa specimen were collected from 40 superficial gastritis patients （20 Hp positive patients and 20 Hp negative patients）, and40 atrophic gastritis patients （20 Hp positive patients and20 Hp negative patients）. The expression ofin- terleukin 17 （IL- 17 ） , toll- like receptor 2 （TLR2） and programmed cell death protein 1 （PD- 1 ） was assessed im- munohistochemistry. Results Patients with Hp positive superficial gastritis showed remarkably higher levels of IL - 17 and PD - 1 than those with Hp negative superficial gastritis （ P 〈 0.05 ）. Patients with Hp positive atrophic gastritis showed remarkably higher levels of IL - 17 and PD - 1 than those with Hp negative atrophic gastritis （ P 〈 0.05 ）. Patients with Hp positive atrophic gastritis showed remarkably higher levels of IL - 17 and PD - 1 than those with Hp posi- tive superficial gastritis （ P 〈 0.05 ）. No statistical difference was found as to TLR2 level in among the groups. Conclu- sion Hp infection can up - regulate the levels of IL - 17 and PD - 1. The progression of patients with Hp infection is related to high expression of IL - 17 and PD - 1, which indicated that IL - 17 and PD - 1 may also cause immunological damage. TLR2 is not involved in immunological responses of Hp infections in the gastric mucosa.