Yamaguchi Hiroyuki, Haranaga Shusaku, Widen Ray, Friedman Herman, Yamamoto Yoshimasa
Department of Medical Microbiology and Immunology, University of South Florida College of Medicine, Tampa, Florida 33612, USA.
Infect Immun. 2002 May;70(5):2392-8. doi: 10.1128/IAI.70.5.2392-2398.2002.
Migration and differentiation of monocytes to the intima of blood vessels may be a crucial first step in the development of atherosclerosis associated with Chlamydia (Chlamydophila) pneumoniae. However, the involvement of C. pneumoniae infection in such steps is not clear. In the present study, therefore, the differentiation-inducing activity of C. pneumoniae to monocytes was examined. Human THP-1 monocytic cell line cells were infected with C. pneumoniae, and the differentiation of monocytes to macrophages was assessed by cell morphology, phagocytic activity, and expression of a cell surface adhesion molecule. The monocytic cells infected with viable bacteria markedly differentiated into macrophages associated with diffused cell morphology, increased uptake of polystyrene beads and increased ICAM-1 (intercellular adhesion molecule 1) expression on the cell surfaces. Heat-killed bacteria did not induce any morphological changes or increase of phagocytosis, but they did induce an increase of cell surface ICAM-1 expressions in THP-1 monocytic cells. The antibiotic minocycline treatment of infected cells resulted in marked inhibition of the cell differentiation as well as C. pneumoniae growth in the cells, but not ICAM-1 expression. In addition, the experiments with human peripheral blood monocytes infected with C. pneumoniae also showed the differentiation of macrophages assessed by morphological change and phagocytic activity. These results indicate that C. pneumoniae infection may directly induce the differentiation of monocytes to macrophages. However, antigenic stimulation of monocytes with bacteria may not be sufficient for a full macrophage differentiation.
单核细胞迁移至血管内膜并分化可能是与肺炎衣原体（嗜衣原体）相关的动脉粥样硬化发展过程中至关重要的第一步。然而，肺炎衣原体感染在这些步骤中的作用尚不清楚。因此，在本研究中，检测了肺炎衣原体对单核细胞的分化诱导活性。用人肺炎衣原体感染人THP-1单核细胞系细胞，并通过细胞形态、吞噬活性和细胞表面黏附分子的表达来评估单核细胞向巨噬细胞的分化。感染活细菌的单核细胞明显分化为巨噬细胞，表现为细胞形态扩散、聚苯乙烯珠摄取增加以及细胞表面细胞间黏附分子1（ICAM-1）表达增加。热灭活细菌未诱导任何形态变化或吞噬作用增加，但它们确实诱导了THP-1单核细胞表面ICAM-1表达增加。用抗生素米诺环素处理感染细胞导致细胞分化以及细胞内肺炎衣原体生长受到明显抑制，但对ICAM-1表达无影响。此外，用人外周血单核细胞感染肺炎衣原体的实验也显示，通过形态变化和吞噬活性评估，巨噬细胞发生了分化。这些结果表明，肺炎衣原体感染可能直接诱导单核细胞分化为巨噬细胞。然而，用细菌对单核细胞进行抗原刺激可能不足以实现巨噬细胞的完全分化。
