Effect of anti-Helicobacter pylori ureB monoclonal antibody on platelet aggregation and activation, and its mechanism study.
- Author:
Yan-yan BAI
1
;
Zhao-yue WANG
;
Xia BAI
;
Jing-cheng MIAO
;
Wei ZHANG
;
Lan DAI
;
Wen-hong SHEN
;
Chang-geng RUAN
Author Information
- Publication Type:Journal Article
- MeSH: Antibodies, Bacterial; pharmacology; Antibodies, Monoclonal; pharmacology; Bacterial Proteins; immunology; metabolism; Helicobacter pylori; immunology; Humans; Integrin beta3; immunology; P-Selectin; immunology; Platelet Activation; drug effects; Platelet Aggregation; drug effects; Urease; immunology; Urokinase-Type Plasminogen Activator; immunology
- From: Chinese Journal of Hematology 2006;27(3):166-169
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVESTo study the effect of monoclonal antibody (McAb) against helicobacter pylori (Hp) ureB, 1F11 on platelet aggregation and activation, and its mechanism.
METHODSThe relativity between human platelet glycoproteins (GPs) and Hp ureB was identified by Western blot and FCM. Platelet aggregation was measured by turbidimetry, and P-selectin and TXB2 assay by ELISA.
RESULTS1F11 could bind to platelet GPIIIa, and ADP-induced platelet aggregation was inhibited by 1F11 in a dose-dependent manner. However, 1F11 had no effect on plasma P-selectin and TXB2 induced by ADP. The FCM results show that the positive rates of platelet binding to FITC-SZ21 was decreased from 99.5% to 77.4% after addition of 1F11.
CONCLUSIONMcAb against Hp ureB 1F11 inhibits platelet aggregation through binding to platelet GPIIIa but does not block platelet activation. There might be crossed-epitopes on Hp ureB and platelet GPIIIa, and Hp infection might be involved in ITP immunopathology.
