The effect of different strains of Helicobacter pylori on platelet aggregation.
OBJECTIVE
Helicobacter pylori is the major causative agent in peptic ulcer disease and is strongly implicated in the development of gastric cancer. It has also been linked, less strongly, to cardiovascular disease. The mechanisms by which certain strains of H pylori induce platelet aggregation through interactions with platelet glycoprotein Ib have been previously described.


METHODS
In the present study, 21 different strains of H pylori, varying in their vacuolating toxin gene, cytotoxic-associated gene A status and other pathogenicity factors, were tested for their ability to induce platelet aggregation.


RESULTS
Ten of the 21 strains induced platelet aggregation, a response that appeared to be independent of their vacuolating toxin gene and cytotoxic-associated gene A status.


CONCLUSIONS
Platelet aggregation has been suggested to be one of the possible mechanisms involved in the effects on the cardiovascular system induced by H pylori. Our results suggest that any putative role H pylori plays in cardiovascular disease may be strain dependent. Further work to identify the H pylori factors involved in induction of platelet aggregation may allow for identification of 'higher risk' strains for cardiovascular disease.
Corcoran
Paul A
PA
Department of Clinical Pharmacology, Royal College of Surgeons in Ireland, Dublin, Ireland.
Atherton
John C
JC
Kerrigan
Steve W
SW
Wadstrom
Torkel
T
Murray
Frank E
FE
Peek
Richard M
RM
Fitzgerald
Desmond J
DJ
Cox
Dermont M
DM
Byrne
Michael F
MF
D000942:Antigens, Bacterial / Q000378:metabolism; D001426:Bacterial Proteins / Q000378:metabolism; D016480:Helicobacter pylori / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D006801:Humans; D066298:In Vitro Techniques; D010974:Platelet Aggregation
D000942:Antigens, Bacterial; D001426:Bacterial Proteins; C074689:VacA protein, Helicobacter pylori; C080866:cagA protein, Helicobacter pylori