Co-Infection with CHLAMYDIA PNEUMONIAE and HELICOBACTER PYLORI Results in Vascular Endothelial Dysfunction and Enhanced VCAM-1 Expression in ApoE-Knockout Mice.

• <i>Background:</i> Upregulation of proinflammatory endothelial cell adhesion molecules and decreased bioactivity of endothelial nitric oxide (NO) are important in the pathogenesis of atherosclerosis. We investigated the effects of co-infection with <i>Chlamydia pneumoniae</i> and <i>Helicobacter pylori </i>on these two events in apoE-KO mice. <i>Methods:</i> Thirty-two apoE-KO mice, 8 weeks old, were equally divided into 4 groups. The first 2 groups were infected with either <i>C. pneumoniae</i> or <i>H. pylori,</i> while the 3rd group was infected with both <i>C. pneumoniae</i> and <i>H. pylori</i>. Mice from the 4th group and 4 wild-type mice served as controls. Thoracic and abdominal aortas were harvested after 10 weeks, and staining for vascular cell adhesion molecule-1 (VCAM-1) and intracellular adhesion molecule-1 was analyzed by immunocytochemistry. The endothelial vasomotor responses of thoracic aortas to methacholine were studied in organ chambers in the absence and presence of <i>L</i>-NAME. The plasma levels of nitrate/nitrite were measured. <i>Results:</i> Staining for VCAM-1 was more intense at the branching sites of aortas from mice with co-infection than in mono-infected or noninfected apoE-KO mice. The relaxation responses to methacholine and the plasma levels of nitrate/nitrite were significantly less in the co-infected group than in the other groups (p < 0.05). <i>Conclusion:</i> Co-infection of apoE-KO mice with <i>C. pneumoniae</i> and <i>H. pylori</i> seems to be associated with impaired bioactivity of endothelial NO and increased expression of VCAM-1 at branching sites. The findings may suggest an additive interaction of these pathogens in atherogenesis.

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MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Kardiologi (hsv//swe)

MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Cardiac and Cardiovascular Systems (hsv//eng)

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