Gaydos C A
Division of Infectious Diseases, Johns Hopkins University, Baltimore, MD 21205.
J Infect Dis. 2000 Jun;181 Suppl 3:S473-8. doi: 10.1086/315612.
The proposed pathogenesis of Chlamydia pneumoniae in atherosclerosis is supported by the finding that C. pneumoniae can initiate and sustain growth in human vascular cells. In vitro growth of C. pneumoniae is found in macrophages, peripheral blood monocyte (PBMC)-derived macrophages, endothelial cells, and aortic artery smooth muscle cells. U-937 macrophages infected with C. pneumoniae are capable of transmitting the infection to human coronary artery endothelial cells (CAEC) with direct cellular contact. Production of cytokines by cells infected with C. pneumoniae indicates that the organism can stimulate the immune system. CAEC infected with C. pneumoniae produce more interleukin-8 than cells sham inoculated with negative control cells. When interferon-gamma is used to stimulate HEp-2 cells, U-937 cells, and PBMC (before infection with C. pneumoniae), inhibition of a productive growth cycle occurs in a dose-related response. Studies are needed to learn the relationship between productive infection and persistence, the ability of C. pneumoniae to affect the immune response, and the potential for C. pneumoniae to influence atheromatous lesions.
肺炎衣原体能够在人类血管细胞中起始并维持生长。在巨噬细胞、外周血单核细胞（PBMC）来源的巨噬细胞、内皮细胞和主动脉平滑肌细胞中发现了肺炎衣原体的体外生长。感染肺炎衣原体的U - 937巨噬细胞能够通过直接细胞接触将感染传播给人冠状动脉内皮细胞（CAEC）。感染肺炎衣原体的细胞产生细胞因子表明该病原体能够刺激免疫系统。感染肺炎衣原体的CAEC比用阴性对照细胞假接种的细胞产生更多的白细胞介素 - 8。当用干扰素 - γ刺激HEp - 2细胞、U - 937细胞和PBMC（在感染肺炎衣原体之前）时，会出现与剂量相关的有效生长周期抑制。需要开展研究以了解有效感染与持续性之间的关系、肺炎衣原体影响免疫反应的能力以及肺炎衣原体影响动脉粥样硬化病变的可能性。
