title: Effects of glucocorticoids on the respiratory burst of Chlamydia-primed THP-1 cells.
abstract: 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.
authors.affiliation: Centre for Oxygen, Research and Development (CORD), Institut de Chimie, B6a, University of Liège, Sart Tilman, 4000 Liège, Belgium. amouithys@ulg.ac.be
authors.forename: Ange
authors.initials: A
authors.lastname: Mouithys-Mickalad
authors.forename: Ginette
authors.initials: G
authors.lastname: Deby-Dupont
authors.forename: Marianne
authors.initials: M
authors.lastname: Mathy-Hartert
authors.forename: Yvette
authors.initials: Y
authors.lastname: Habraken
authors.forename: Monique
authors.initials: M
authors.lastname: Nys
authors.forename: Yves
authors.initials: Y
authors.lastname: Henrotin
authors.forename: Maurice
authors.initials: M
authors.lastname: Lamy
authors.forename: Carol
authors.initials: C
authors.lastname: Deby
mesh_terms: D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D002454:Cell Differentiation; D002460:Cell Line; D016993:Chlamydophila pneumoniae / Q000378:metabolism / Q000472:pathogenicity / Q000502:physiology*; D004578:Electron Spin Resonance Spectroscopy; D005030:Ethylenes / Q000096:biosynthesis; D015870:Gene Expression / Q000187:drug effects; D006801:Humans; D006854:Hydrocortisone / Q000494:pharmacology*; D006861:Hydrogen Peroxide / Q000378:metabolism; D016209:Interleukin-8 / Q000037:antagonists & inhibitors / Q000096:biosynthesis; D026901:Membrane Transport Proteins / Q000096:biosynthesis; D008775:Methylprednisolone / Q000494:pharmacology*; D009000:Monocytes / Q000166:cytology / Q000187:drug effects / Q000378:metabolism* / Q000382:microbiology*; D009252:NADPH Dehydrogenase / Q000096:biosynthesis; D019255:NADPH Oxidases; D016328:NF-kappa B / Q000378:metabolism; D010750:Phosphoproteins / Q000096:biosynthesis; D017382:Reactive Oxygen Species / Q000378:metabolism; D016897:Respiratory Burst / Q000187:drug effects* / Q000502:physiology; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D005030:Ethylenes; D016209:Interleukin-8; D026901:Membrane Transport Proteins; D016328:NF-kappa B; D010750:Phosphoproteins; D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha; D006861:Hydrogen Peroxide; D019255:NADPH Oxidases; C086986:CYBA protein, human; D009252:NADPH Dehydrogenase; D006854:Hydrocortisone; D008775:Methylprednisolone