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Blood, 1 February 2007, Vol. 109, No. 3, pp. 1265-1274.
Prepublished online as a Blood First Edition Paper on October 3, 2006; DOI 10.1182/blood-2006-02-001115.
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Submitted February 2, 2006
Accepted June 13, 2006
Glucocorticoids induce differentiation of a specifically
activated, anti-inflammatory subtype of human monocytes
Jan Ehrchen, Lars Steinmuller, Katarzyna Barczyk, Klaus Tenbrock, Wolfgang Nacken, Martin Eisenacher, Ursula Nordhues, Clemens Sorg, Cord Sunderkotter, and Johannes Roth*
Institute of Experimental Dermatology, University of Muenster, Germany
Interdisciplinary Center for Clinical Research, University of Muenster, Germany
Department of Dermatology, University of Muenster, Germany
* Corresponding author; email: rothj{at}uni-muenster.de.
Monocytes and macrophages may either promote or down-regulate inflammatory reactions depending on their state of activation. The effects of glucocorticoids (GC), the most widely used immunosuppressive drugs, on monocytes are currently not well defined. Analyzing the GC-induced expression pattern in human monocytes by microarray technology we identified for the first time GC-dependent regulation of 133 genes, including anti-inflammatory molecules like adenosine A3 receptor, CD1d, and IL1 receptor II. The results were independently confirmed by real-time PCR and flow cytometry. Functional clustering of GC-regulated genes indicated induction of monocytic properties like " phagocytosis" and " motility" as well as repression of "adhesion", " apoptosis" and " oxidative burst" . These predictions were confirmed by independent functional assays. GC up-regulate fMLP receptors and specifically promote chemotaxis to this chemoattractant. Furthermore, GC promote survival of an anti-inflammatory monocytic phenotype in inflammatory reactions probably by inhibition of apoptosis due to oxidative stress. GC limit tissue damage due to induction of anti-oxidative properties and high capacity for phagocytosis of pro-inflammatory agents. Thus, GC-treatment did not cause a global suppression of monocytic effector functions but results in differentiation of a specific anti-inflammatory phenotype which seems to be actively involved in resolution of inflammatory reactions.
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