Biochemical and Biophysical Research Communications, Vol.318, No.4, 941-948, 2004
Effects of glucocorticoids on the respiratory burst of Chlamydia-primed THP-1 cells
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. (C) 2004 Elsevier Inc. All rights reserved.
Keywords:monocytes;Chlamydia pneumoniae;hydrocortisone;methylprednisolone;NADPH-oxidase;IL-8;TNF alpha;NF-KB;priming