Social stress and the regulation of tumor necrosis factor-alpha secretion

Abstract

Social disruption (SDR), a murine model of social stress, altered the phenotype and function of spleen immune cells. Previous reports indicated that following SDR spleens contained higher numbers of CD11b+ monocytes, and these cells were less sensitive to the inhibitory effects of glucocorticoids on cell viability. Additionally, lipopolysaccharide (LPS)-stimulated splenocytes from SDR mice secreted higher levels of the proinflammatory cytokines tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 compared to splenocytes from controls. The present study sought to further examine the effects of SDR on TNFalpha secretion from splenocytes. We report that SDR increased TNFalpha secretion from an enriched fraction of CD11b+ monocytes stimulated with LPS. Additionally, SDR altered the kinetics of TNFalpha release from LPS-stimulated splenocytes and induced minor changes in the suppressive effects of corticosterone and norepinephrine on LPS-induced TNFalpha secretion. These results are in agreement with the notion that complex interactions mediate the response to social stress.