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International Journal of Endocrinology
Volume 2013, Article ID 405127, 9 pages
http://dx.doi.org/10.1155/2013/405127
Research Article

Low Concentrations of Corticosterone Exert Stimulatory Effects on Macrophage Function in a Manner Dependent on Glucocorticoid Receptors

1Department of Anesthesiology, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, China
2State Key Laboratory of Trauma, Burns, and Combined Injury, Research Institute of Surgery, Daping Hospital, Third Military Medical University, Chongqing 400042, China
3Medical Department, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, China

Received 14 June 2013; Revised 24 August 2013; Accepted 25 August 2013

Academic Editor: Mario Maggi

Copyright © 2013 He-Jiang Zhong et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Endogenous glucocorticoids (GCs) have both stimulatory and suppressive effects on immune cells depending on the concentration. However, the mechanisms underlying the stimulatory effects of GCs remain elusive. Rat peritoneal macrophages were treated with different concentrations of corticosterone (0, 30 nM, 150 nM, and 3 μM). To inhibit the glucocorticoid receptor (GR) activity, macrophages were preincubated with the GR antagonist RU486 (mifepristone, 10 μM) for 30 min before treatment with corticosterone (150 nM). In the absence of immune stimuli, the chemotactic and phagocytic activities of macrophages were markedly enhanced by low concentrations of corticosterone (30 and 150 nM) when compared with vehicle-treated controls. However, these effects were not observed at a high concentration of corticosterone (3 μM). Furthermore, blocking GR activity inhibited 150 nM corticosterone-enhanced chemotaxis and phagocytosis of macrophages. Meanwhile, after treatment with corticosterone (150 nM) for 1 h and 3 h, GR protein expression increased to 1.4- and 2.2-fold, respectively, compared to untreated macrophages. These effects were inhibited by RU486. However, mineralocorticoid receptor (MR) protein expression was not influenced by 150 nM corticosterone. These results demonstrate that low concentrations of corticosterone exert stimulatory effects on macrophage function in the absence of immune stimuli, and GR is at least partially responsible for these effects.