This study shows that C. pneumoniae infection enhances the inflammatory process by increasing T-lymphocytes in the plaque and accelerates the formation of complex lesions.
Background and Purpose-Chlamydia pneumoniae has repeatedly been associated with atherosclerotic disease. Our study was designed to clarify whether this association is based on C pneumoniae-induced transformation of a stable into an unstable atherosclerotic plaque or on stimulation of hypercoagulability leading to increased thrombotic arterial occlusions by C pneumoniae infection. Transcranial Doppler ultrasonographic monitoring of the middle cerebral artery during carotid endarterectomy offers the opportunity to study, before removal of the plaque, atherothrombotic emboli dislodging from an unstable carotid plaque (plaque-related emboli) and emboli related to (excessive) thrombus formation at the endarterectomy site after removal of the plaque and restoration of flow (thrombosis-related emboli). Methods-C pneumoniae IgA (Ն1/16) and IgG (Ն1/64) seropositivity was assessed in 53 patients with symptomatic carotid artery disease undergoing carotid endarterectomy. The removed carotid plaques were studied histologically to assess plaque instability. Results-Plaque-and thrombosis-related emboli were registered in 43 patients with an adequate transtemporal window.IgA seropositivity (58%) was associated significantly with thrombosis-related embolization (Pϭ0.030) but not with plaque-related embolization or with histological plaque instability. Conclusions-C pneumoniae serology is associated with microembolization after endarterectomy and restoration of flow.Since these microemboli represent platelet aggregations and are related to cerebrovascular complications, our data suggest that C pneumoniae infection contributes to cerebrovascular events in patients with carotid artery disease through stimulation of thrombosis.
Multiple reports have demonstrated an association between Chlamydia pneumoniae (Cpn) and cardiovascular disease. In this study we evaluated the effect of Cpn infections on early lesion progression in C57BL/6J mice. Since plaque formation in these mice does not develop past the initial stage, we thought these mice might be a better model for unravelling the effect of Cpn infection on early lesion type progression. C57BL/6J mice were fed an atherogenic diet and injected 10 times with 5 x 10(7) IFU Cpn or mock. At sacrifice, lesion number, size and type were analysed. To study the role of Cpn in inflammation, serum amyloid P (SAP) in plasma was determined as well as T-cells, macrophages and SAP in the lesions. In the aortic sinus of both groups, type 2 lesions were found. Cpn infection resulted in a 2.2-fold increase in total lesion size (Cpn: 10821+/-2429 microm(2)vs mock: 5022+/-1348 microm(2); p=0.04). No difference in lesion number was observed. Also, Cpn infection increased SAP in the lesions from 1.10(-4)+/-0.1.10(-4) SAP-positive cells/lesion area to 10.10(-4)+/-1.10(-4) SAP-positive cells/lesion area (p=0.05). The influx of T-lymphocytes and macrophages in the lesions as well as SAP plasma levels were not different between groups. Multiple Cpn infections resulted in a significant increase in total lesion size of C57BL/6J mice. Increase in total SAP-positive area in infected mice suggests a role for this acute-phase protein in lesion enlargement.
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