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Helicobacter pylori upregulates endothelial adhesion molecules but the pattern is unclear. Human umbilical vein endothelial cells (HUVEC) were exposed to control medium or H. pylori 60190. Binding of monoclonal antibodies against P-selectin, E-selectin, vascular adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) was determined using enzyme-linked immunosorbent assay. Binding of polymorphonuclear leukocytes to HUVEC was determined on cells exposed as above. After 6 h exposure to H. pylori, there were 30%, 124%, 167% and 100% increases in P-selectin, E-selectin, VCAM-1 and ICAM-1 levels and a 400% increase in polymorphonuclear leukocyte adhesion in HUVEC exposed to H. pylori. Effects of incubation for other intervals between 0 and 18 h are also described. H. pylori exerts some of its effects on gastric mucosa via gastric vasculature. This study gives insight into the pattern of H. pylori-associated endothelial adhesion molecule upregulation. [Copyright &y& Elsevier]

Background: Clinical studies have suggested an association between cardiovascular disease and infection with H pylori. We have described strain specific H pylori-induced platelet aggregation that involves platelet glycoprotein lb and van Willebrand factor (vWf). We exam ned the role of H pylori antibodies in this aggregation. Methods and Results: Addition of pooled immunoglobin (Ig) and fibrinogen along with H pylori strain 60190 (coated in vWf) to washed platelets led to platelet aggregation (60±4% n=3). Antibodes involved were specific to H pylori as bacteria incubated in pooled g and subsequently washed could support platelet aggregation (49±7%, n=3). To confirm this, pooled Ig was incubated with H pylori or Streptococcus sanguis. Bacteria were removed by centrifugation and the depleted g used in aggregation assays. H pylori-depleted Ig showed greatly reduced platelet aggregation to H pylori (13±9%, n=3, p<0.01) while the S sanguis-depleted Ig was not affected (54±3%, n=3, p=NS). All 20 plasma donors were tested for H pylori seropositivity using a H pylori ELISA. All 4/4 of the positive volunteers consistent y aggregated in response to H pylori while only 2/15 of the H pylori negative donors aggregated consistently (p=0.039, Fisher's Exact Test). The relative risk of H pylori positivity for aggregation was 7.5 (CI 2.0-27.3). Conclusions: H pylori-induced platelet aggregation requires binding of H pylori-specific IgG. This pro-aggregatory phenotype is not unique to H pylori and has been described with S sanguis and P gingivalis. Exposure to oral bacteria such as S sanguis can lead to infective endocarditis and in the case of P gingivalis, to enhancement of atherosclerosis in animal models. Repeated exposure to proaggregatory bacteria such as certain strains of H pylori may not cause coronary artery disease but could accelerate the progression of the disease. Local platelet effects may also contribute to the pathogenesis of H... [ABSTRACT FROM AUTHOR]