H Pylori
Copyright ©The Author(s) 2004. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jul 15, 2004; 10(14): 2055-2059
Published online Jul 15, 2004. doi: 10.3748/wjg.v10.i14.2055
Helicobacter pylori lipopolysaccharide: Biological activities in vitro and in vivo, pathological correlation to human chronic gastritis and peptic ulcer
Yi-Hui Luo, Jie Yan, Ya-Fei Mao
Yi-Hui Luo, Jie Yan, Ya-Fei Mao, Department of Medical Microbiology and Parasitology, College of Medical Science, Zhejiang University, Hangzhou 310031, Zhejiang Province, China
Author contributions: All authors contributed equally to the work.
Supported by the Foundation of Ministry of Education of China for Distinguished Young Scholars
Correspondence to: Professor Jie Yan, Department of Medical Microbiology and Parasitology, College of Medical Science, Zhejiang University, 353 Yan An Road, Hangzhou 310031, Zhejiang Province, China. yanchen@mail.hz.zj.cn
Telephone: +86-571-87217385 Fax: +86-571-87217044
Received: December 23, 2003
Revised: January 3, 2004
Accepted: January 12, 2004
Published online: July 15, 2004
Abstract

AIM: To determine the biological activity of Helicobacter pylori (H pylori) lipopolysaccharide (H-LPS) and understand pathological correlation between H-LPS and human chronic gastritis and peptic ulcer.

METHODS: H-LPS of a clinical H pylori strain and LPS of Escherichia coli strain O55:B5 (E-LPS) were extracted by phenol-water method. Biological activities of H-LPS and E-LPS were detected by limulus lysate assay, pyrogen assay, blood pressure test and PBMC induction test in rabbits, cytotoxicity test in NIH 3T3 fibroblast cells and lethality test in NIH mice. By using self-prepared rabbit anti-H-LPS serum as the first antibody and commercial HRP-labeled sheep anti-rabbit sera as the second antibody, H-LPS in biopsy specimens from 126 patients with chronic gastritis (68 cases) or gastric ulcer (58 cases) were examined by immunohistochemistry.

RESULTS: Fibroblast cytotoxicity and mouse lethality of H-LPS were weaker than those of E-LPS. But the ability of coagulating limulus lysate of the two LPSs was similar (+/0.5 ng/mL). At 0.5 h after H-LPS injection, the blood pressures of the 3 rabbits rapidly declined. At 1.0 h after H-LPS injection, the blood pressures in 2 of the 3 rabbits fell to zero causing death of the 2 animals. For the other one rabbit in the same group, its blood pressure gradually elevated. At 0.5 h after E-LPS injection, the blood pressures of the three rabbits also quickly declined and then maintained at low level for approximately 1.0 h. At 0.5 h after injection with H-LPS or E-LPS, PBMC numbers of the rabbits showed a remarkable increase. The total positivity rate of H-LPS from 126 biopsy specimens was 60.3% (76/126). H-LPS positivity rate in the biopsy specimens from chronic gastritis (50/68, 73.5%) was significantly higher than that from gastric ulcer (26/58, 44.8%) (χ2 = 10.77, P < 0.01). H-LPS positivity rates in biopsy specimens from chronic superficial gastritis (38/48, 79.2%) and chronic active gastritis (9/10, 90.0%) were significantly higher than that of the patients with atrophic gastritis (3/10, 30.0%) (χ2 = 7.50-9.66, P < 0.01).

CONCLUSION: The biological activities of H-LPS were weaker than those of E-LPS, the activities of H-LPS of lowering rabbit blood pressure and inducing rabbit PBMC were relatively stronger. H-LPS may play a critical role in inducing inflammatory reaction in human gastritis.

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