Interleukin-6 and the development of social disruption-induced glucocorticoid resistance

Jennifer L. Stark, Ronit Avitsur, John Hunzeker, David A. Padgett, John F. Sheridan

Research output: Contribution to journalArticlepeer-review

90 Scopus citations

Abstract

Following social disruption (SDR) stress in male mice, corticosterone resistance of splenocytes was accompanied by enhanced LPS-stimulated interleukin (IL)-6 secretion. The present study examined the role of IL-6 in the development of corticosterone resistance. Addition of IL-6 to control splenocyte cultures did not induce corticosterone resistance. SDR also elevated IL-6 in plasma and liver, but not in spleen. IL-6 deficient mice that were exposed to SDR developed glucocorticoid resistance despite the absence of systemic IL-6. These findings suggest that although SDR enhanced IL-6 responses, IL-6 was not essential for the development of stress-induced splenocyte corticosterone resistance.

Original languageEnglish (US)
Pages (from-to)9-15
Number of pages7
JournalJournal of Neuroimmunology
Volume124
Issue number1-2
DOIs
StatePublished - 2002

Bibliographical note

Funding Information:
We are grateful to Dr. F. Michael Beck for assistance with statistical analyses. We thank Kari Kramer and Patty Guerra for help with the animal work and Kari Kramer for excellent technical assistance with the IL-6 ELISA. These studies were supported by grants from the NIMH (F31 MH11792 to J.L.S. and RO1 MH46801-08 to J.F.S.), and the John D. and Catherine T. MacArthur Foundation Mind-Body Network.

Keywords

  • Corticosterone resistance
  • Lipopolysaccharide
  • Liver
  • Mice
  • Spleen
  • Stress

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