目的 探讨幽门螺杆菌(Hp)相关性胃炎患者胃粘膜内趋化因子IP-10、Mig的表达水平.方法 28例胃炎患者行胃镜检查钳取胃粘膜标本,依据HE染色、快速尿素酶试验及石炭酸染色,分为正常胃粘膜组、Hp阴性胃炎组及Hp阳性胃炎组,并对Hp阳性胃炎组的炎症活动程度进行分级.以ELISA法检测胃粘膜内IP-10、Mig的表达水平.结果 正常对照组、Hp阴性组、Hp阳性组的IP-10、Mig含量分别为(30.5±14.6)、(60.4±23.8)、(179.9±30.2)ng·L-1和(24.1±14.4)、(49.5±19.4)、(160.6±34.6)ng·L-1,与正常对照组相比,差异显著(分别为P<0.05、P<0.01),且Hp阳性组IP-10、Mig的表达水平与胃粘膜炎症活动程度均呈正相关(r＝0.9811,P<0.001和r＝0.9938,P<0.001).结论 IP-10、Mig介导了Hp相关性胃炎炎症细胞的浸润,造成胃粘膜组织损伤,在Hp相关性胃炎发病机制中起一定作用.%In order to study the expression of chemokine interferon γ- inducible protein 10(IP-10)and monokine inducible by γ interferon(Mig)in patients with gastritis induced by Helicobacter pylori (Hp), gastric mucosa specimens from 28 cases obtained by gastroscope were divided into normal control group, Hp (+) group and Hp (-) group according to the methods of hematoxylin and erosin( HE)staining, rapid urease test(RUT)and carbolic acid staining. And the gastric mucosa specimens of Hp (+) group were degreed in terms of gastric mucosa inflammation. The expression of IP-10 and Mig in patients with gastritis was measured by enzyme linked immunosorbent assay (ELISA). The expression of IP-10 in normal control group, HP(-)group and HP(+) group were (30. 5±14.6), (60. 4±23. 8)and(179.9±30.2)ng · L-1. Simultaneously the expression of Mig in these ghree groups were(24. 1±1.4), (49.5 ± 19.4) and (160. 6±34.6) ng · L-1 , respectively. It was significant difference higher in patients than that in normal controls (P＜0.05 ,P＜0.01), and the expression of IP-10 and Mig in patients with gastritis induced by Hp were quite correlated with the degree of gastric mucosa inflammation (r= 0. 9811, P＜0.001 and r=0. 9938, P＜0. 001). Results demonstrated that the chemokine IP-10 and Mig play an important role in trafficking inflammatory cells to gastric mucosa, mediating the development of gastritis induced by Hp.
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