Airenne S, Surcel H M, Alakärppä H, Laitinen K, Paavonen J, Saikku P, Laurila A
National Public Health Institute, Oulu, Helsinki, Finland.
Infect Immun. 1999 Mar;67(3):1445-9. doi: 10.1128/IAI.67.3.1445-1449.1999.
Chlamydia pneumoniae infection has been associated with cardiovascular diseases in seroepidemiological studies and by demonstration of the pathogen in atherosclerotic lesions. It has the capacity to infect several cell types, including monocyte-derived macrophages, which play an essential role in the development of atherosclerosis. However, the persistence of C. pneumoniae in mononuclear cells is poorly understood. To study the morphology and biological characteristics of the infection, human peripheral blood monocytes were infected with C. pneumoniae. Freshly isolated monocytes resisted the development of infectious progeny, and confocal and transmission electron microscopy showed that the morphology of the inclusions and chlamydial particles was abnormal. Addition of tryptophan or antibodies against gamma interferon did not diminish the inhibition of C. pneumoniae, suggesting that other factors are involved in the chlamydiostatic activity of the monocytes. Chlamydial mRNA was expressed at least 3 days after infection, however, and a capability for infected monocytes to induce a positive lymphocyte proliferative response was detected for up to 7 days, indicating that C. pneumoniae remains metabolically active in the monocytes in vitro. These results are in accordance with the hypothesis that C. pneumoniae may participate in the maintenance of local immunological response and inflammation via infected monocytes and thus enhance atherosclerosis.
在血清流行病学研究以及通过在动脉粥样硬化病变中证实病原体后,肺炎衣原体感染已与心血管疾病相关联。它有能力感染多种细胞类型,包括单核细胞衍生的巨噬细胞,而这些巨噬细胞在动脉粥样硬化的发展中起着至关重要的作用。然而,人们对肺炎衣原体在单核细胞中的持续存在了解甚少。为了研究感染的形态和生物学特性,用肺炎衣原体感染了人类外周血单核细胞。新鲜分离的单核细胞抑制感染性后代的产生,共聚焦显微镜和透射电子显微镜显示包涵体和衣原体颗粒的形态异常。添加色氨酸或抗γ干扰素抗体并没有减少对肺炎衣原体的抑制作用,这表明其他因素参与了单核细胞的衣原体生长抑制活性。然而,衣原体mRNA在感染后至少3天表达,并且检测到感染的单核细胞诱导阳性淋巴细胞增殖反应的能力长达7天,这表明肺炎衣原体在体外单核细胞中仍保持代谢活性。这些结果与以下假设一致,即肺炎衣原体可能通过感染的单核细胞参与局部免疫反应和炎症的维持,从而加重动脉粥样硬化。