Chlamydia pneumoniae infections augment atherosclerotic lesion formation: a role for serum amyloid P
Abstract:Ezzahiri R, Stassen FRM, Kurvers HRM, Dolmans V , Kitslaar PJEHM, Bruggeman CA. Chlamydia pneumoniae infections augment atherosclerotic lesion formation: a role for serum amyloid P. APMIS 2006;114:117–26.
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 · 107 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 μm2vs mock: 5022±1348 μm2; 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.
Document Type: Research Article
Publication date: February 1, 2006