Chlamydia pneumoniae infection induces differentiation of monocytes into macrophages.
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.
Yamaguchi
Hiroyuki
H
Department of Medical Microbiology and Immunology, University of South Florida College of Medicine, Tampa, Florida 33612, USA.
Haranaga
Shusaku
S
Widen
Ray
R
Friedman
Herman
H
Yamamoto
Yoshimasa
Y
D001161:Arteriosclerosis / Q000209:etiology; D002454:Cell Differentiation / Q000187:drug effects; D002455:Cell Division; D002460:Cell Line; D016993:Chlamydophila pneumoniae / Q000472:pathogenicity*; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis; D008264:Macrophages / Q000502:physiology*; D008911:Minocycline / Q000494:pharmacology; D009000:Monocytes / Q000502:physiology*; D010586:Phagocytes / Q000502:physiology; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology
D018799:Intercellular Adhesion Molecule-1; D008911:Minocycline; D013755:Tetradecanoylphorbol Acetate