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Originally published online as doi:10.1189/jlb.0303090 on July 15, 2003

Published online before print July 15, 2003
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(Journal of Leukocyte Biology. 2003;74:507-513.)
© 2003 by Society for Leukocyte Biology

Expression of glucocorticoid resistance following social stress requires a second signal

Ronit Avitsur*, David A. Padgett*,{dagger},{ddagger}, Firdaus S. Dhabhar*,{dagger},{ddagger}, Jennifer L. Stark*, Kari A. Kramer*, Harald Engler* and John F. Sheridan*,{dagger},{ddagger},1

* Section of Oral Biology,
{dagger} Department of Molecular Virology, Immunology and Medical Genetics,
{ddagger} The Institute for Behavioral Medicine Research, The Ohio State University, Columbus

1Correspondence: Ohio State University, College of Dentistry, Section of Oral Biology, 305 West 12th Ave., P.O. Box 182357, Columbus, OH 43218-2357. E-mail: sheridan.1{at}osu.edu

Stimulation of splenocytes from socially stressed mice [social disruption (SDR)] with Gram-negative bacterial lipopolysaccharide (LPS) revealed a state of functional glucocorticoid (GC) resistance. LPS-stimulated splenocytes were less sensitive to the inhibitory effects of corticosterone. This study demonstrated that activation signals were required for the expression of splenic GC resistance. The results demonstrated that six cycles of SDR induced splenomegaly and increased the number of CD11b-positive monocytes. SDR also increased the viability of cultured, nonstimulated splenocytes, and addition of corticosterone reduced the viability of these cells in a dose-dependent manner. However, following stimulation with LPS, the sensitivity of SDR splenocytes to GC was reduced. Similar results were obtained using lipid A, a fraction of the LPS molecule that binds to Toll-like receptor (TLR)4. Furthermore, C3H/HeJ mice that do not possess a functional TLR4 molecule responded to SDR with an increased number of CD11b-positive monocytes in the spleen and increased viability of nonstimulated splenocytes. However, neither LPS nor lipid A stimulation resulted in the expression of GC resistance. Together, these findings suggest that the expression of GC resistance in response to SDR requires a second signal that can be provided by ligation of TLR4.

Key Words: social disruption (SDR) • lipopolysaccharide • monocytes/macrophages • CD11b • C3H/HeJ




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