Chlamydia pneumoniae induces chemokine expression by platelets in patients with atherosclerosis

In this study, the role of Chlamydia pneumoniae in triggering platelets to induce the inflammatory potential chemokines CCL3, CCL5, CCL7 and CXCL8 in atherosclerotic patients was investigated. Venous blood from control subjects [n=35] and atherosclerotic patients [n=35] was collected in tubes with and without EDTA. Platelets from controls and patients were separated from whole blood and then stimulated with lipopolysaccharide [LPS], live C. pneumoniae and heat-treated C. pneumoniae. The ability of C. pneumoniae and its LPS to stimulate platelets and expression of CCL3, CCL5, CCL7 and CXCL8 was assessed with immunofluorescence. Immunosorbent assays were used to detect anti-C. pneumoniae antibodies in sera from patients and healthy subjects. Nonstimulated platelets from patients showed significant expression of CCL3, CCL5, CCL7 and CXCL8 compared to controls [p<0.0001]. Stimulation of platelets from patients with live and heat-treated C. pneumoniae and its LPS demonstrated significant induction of chemokines compared to similarly stimulated platelets from controls [p<0.01]. After stimulation with heat-treated C. pneumoniae chemokine expression in platelets from controls was significantly lower than after stimulation with live C. pneumoniae [p<0.01], which was not the case when platelets from patients were stimulated. Increased levels of anti-C. pneumoniae antibodies were detected in sera from patients compared to healthy subjects, suggesting prior C. pneumoniae exposure. Our data demonstrated an interactive link between C. pneumoniae and platelets in atherosclerotic patients, leading to induction of potential chemokines and possibly disease development

Acute ischemic brain stroke is associated with the consequences of Chlamydia pneumoniae infection

Ischemic brain Stroke is associated with chronic inflammation and elevation of several cytokines such as Tumor Necrosis Factor alpha [TNF-alpha] and Interleukin [IL]-8 [IL-8] which are correlated with CNS injury and stroke.Chlamydia pneumoniae [CP] was suggested to be an independent riskfactor for stroke. Atherosclerosis may be a manifestation of chronic or persistent CP infection in the atherosclerotic plaque. To investigate the effect of live CP and chlamydial lipopolysaccharide [LPS] on the production of TNF-alpha and IL-8, and to study the levels of anti-CP IgG antibodies in the first acute ischemic stroke patients. Venous blood samples were collected in EDTA tubes from patients who had first time acute ischemic stroke [n=14] and from healthy subjects [controls] [n=14]. Leukocytes were isolated and cultured either non-stimulated or stimulated with chlamydial LPS and live CP. Intracellular cytokine production was detected by immunocytochemistry. Anti-CP IgG and IgA antibodies were detected by enzyme immunoassay [EIA]. The data showed significant increase of chlamydial stimulated and non-stimulated TNF-alpha and IL-8 production in patients compared to control [P<0.03]. There were a significant increase in anti-CP IgG antibodies in stroke patients compared to controls [P<0.0001]. The study concluded that pathological changes in acute brain stroke might be a consequence of CP infections that mediated induction of potential proinflammatory cytokines