Keywords :
Anti-Inflammatory Agents/pharmacology; Cell Differentiation; Cell Line; Chlamydophila pneumoniae/metabolism/pathogenicity/physiology; Electron Spin Resonance Spectroscopy; Ethylenes/biosynthesis; Gene Expression/drug effects; Humans; Hydrocortisone/pharmacology; Hydrogen Peroxide/metabolism; Interleukin-8/antagonists & inhibitors/biosynthesis; Membrane Transport Proteins/biosynthesis; Methylprednisolone/pharmacology; Monocytes/cytology/drug effects/metabolism/microbiology; NADPH Dehydrogenase/biosynthesis; NADPH Oxidase; NF-kappa B/metabolism; Phosphoproteins/biosynthesis; Reactive Oxygen Species/metabolism; Respiratory Burst/drug effects/physiology; Tumor Necrosis Factor-alpha/antagonists & inhibitors/metabolism
Abstract :
[en] We previously observed that the respiratory burst of human monocytes (THP-1 cell line) triggered by phorbol myristate acetate was strongly enhanced by a priming of the cells by Chlamydia pneumoniae [Biochem. Biophys. Res. Commun. 287 (2001) 781]. We describe here the modifications of the responses of Chlamydia-primed THP-1 cells to hydrocortisone (HCT) and methylprednisolone (MPL). HCT and MPL inhibited the production of the cytokines TNFalpha and IL-8. But HCT, which inhibited the respiratory burst in LPS-primed monocytes, paradoxically stimulated the phenomenon in Chlamydia-primed cells; MPL exerted no significant effect. Both glucocorticoids did not significantly modify the triggering effect of Chlamydia on NF-kappaB binding activity. On the expression of p22(phox), a protein subunit of the NADPH oxidase, HCT had an increasing and MPL a decreasing effect. Glucocorticoids thus had unexpected effects on the inflammatory response of Chlamydia-primed monocytes.
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