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

• Published in: Journal of neuroimmunology Vol. 124; no. 1; pp. 9 - 15
• Main Authors: Stark, Jennifer L, Avitsur, Ronit, Hunzeker, John, Padgett, David A, Sheridan, John F
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.03.2002
• Subjects: Animals; Corticosterone - pharmacology; Corticosterone resistance; Drug Resistance; Interleukin-6 - pharmacology; Interleukin-6 - physiology; Interpersonal Relations; Lipopolysaccharide; Lipopolysaccharides - pharmacology; Liver; Male; Mice; Mice, Inbred C57BL; Spleen; Spleen - cytology; Spleen - drug effects; Spleen - physiopathology; Stress; Stress, Psychological - etiology; Stress, Psychological - physiopathology; Spleen; Lipopolysaccharide; Corticosterone resistance; Mice; Liver; Stress
• ISSN: 0165-5728; 1872-8421
• DOI: 10.1016/S0165-5728(02)00004-8

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.