Effect of Helicobacter pylori infection on macrophage migration inhibitory factor protein expression in patients with chronic gastritis and gastric ulcer precancerous lesions
- VernacularTitle:根除幽门螺杆菌对慢性胃炎和胃溃疡组织中MIF蛋白表达的影响
- Author:
Shuangxia ZHANG
;
Guangdi LI
;
Xiaohui YU
;
Fangxin ZHANG
- Publication Type:Journal Article
- Keywords:
macrophage migration inhibitory factor;
Helicobacter pylori;
chronic gastritis;
gastric ulcer
- From:
Journal of Xi'an Jiaotong University(Medical Sciences)
2009;30(6):724-728
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of Helicobacter pylori (Hp) infection on macrophage migration inhibitory factor (MIF) protein expression and explore the role of Hp and MIF in the development of chronic gastritis and gastric ulcer. Methods The biopsy tissues of gastric mucosa were collected under gastroscope, and Hp was detected by 14C breath test and Warthin-starry method. We recruited 25 healthy people with normal gastric mucosa, 40 patients pathologically confirmed Hp-positive with chronic superficial gastritis, 40 with atrophic gastritis and 40 with gastric ulcer. MIF protein expression was examined by immunohistochemical SP staining method, then Hp eradication was performed on Hp-infected chronic superficial gastritis, atrophic gastritis and gastric ulcer for 2 weeks. Hp and MIF were re-examined 4 weeks after drug withdrawal, and difference in MIF expression was compared between Hp-infected patients and Hp-eradicated patients. Results The expression of MIF was low in normal gastric mucosa without Hp infection (2/25, 8%), but significantly higher in Hp-infected gastric mucosa with chronic superficial gastritis (12/40, 30%), atrophic gastritis (26/40, 65%) and gastric ulcer (19/40, 47.5%); there was a significant difference between normal gastric mucosa without Hp infection and that of comHp-infected patients (57/120 vs. 2/25; χ~2=13.376, P<0.01). MIF expression increased with the severity of inflammation in chronic gastritis, and there was a significant difference between superficial gastritis and atrophic gastritis (12/40 vs. 26/40; χ~2=9.825, P<0.01). The expression of MIF was noticeably decreased after Hp eradication compared with before(57/120 vs. 23/103; χ~2=15.264, P<0.01); however, there was no significant change in those patients whose Hp was still positive. Conclusion The expression of MIF on gastric mucosa is associated with the development of chronic gastritis and gastritis ulcer caused by Hp infection. Eradication of Hp could cut down the abnormally high MIF expression in gastric mucosa and slow down the formation and development of gastric carcinoma.
