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Abstract
Mice exposed to chronic subordinate colony housing (CSC) stress show glucocorticoid (GC) resistance of in vitro lipopolysaccharide (LPS)-stimulated splenocytes, increased anxiety and colitis. Similar effects were reported in wounded mice exposed to social disruption (SDR). Here we show that CSC exposure induced GC resistance in isolated and in vitro LPS-stimulated, but not unstimulated, splenocytes, and these effects were absent when CD11b+ splenocytes were depleted. Moreover, re-active coping behaviour during CSC correlated with the attacks and bites received by the resident, which in turn highly correlated with the dimension of splenic GC resistance, as with basal and LPS-induced in vitro splenocyte viability. Importantly, social stress promoted spleen cell activation, independent of bite wounds or CD11b+/CD11b− cell phenotype, whereas GC resistance was dependent on both bite wounds and the presence of CD11b+ cells. Together, our findings indicate that the mechanisms underlying splenic immune activation and GC resistance following social stress in male mice are paradigm independent and, to a large extent, dependent on wounding, which, in turn, is associated with a re-active coping style.
Highlights
Chronically-stressed individuals run the risk for developing numerous somatic and affective disorders[1,2], of which most are associated with an activated immune status and chronic low-grade inflammation[3,4,5]
Statistical analysis revealed no differences in body weight gain (Fig. 2A) between chronic subordinate colony housing (CSC) (n = 23) and single housed control (SHC; n = 24) mice
Identical effects of CSC on adrenal and thymus weight have been reported for the remaining SHC (n = 24) and CSC (n = 23) mice used in this study[30,31]
Summary
Chronically-stressed individuals run the risk for developing numerous somatic and affective disorders[1,2], of which most are associated with an activated immune status and chronic low-grade inflammation[3,4,5]. A lack of GC resistance following immobilisation stress[18] initially suggested this phenomenon to be specific for social stressors, it rather seems as if the occurrence of skin injuries paralleling a certain social stressor, which in contrast to humans poses a common phenomenon in animals, and not the social character of the stressor per se, is critical for splenic immune activation and GC resistance Support for this hypothesis is provided by the finding that splenocytes of wounded SDR mice produced more cytokines in response to LPS stimulation and showed a lower sensitivity to corticosterone (CORT) compared with mice exposed to a milder social stress paradigm preventing direct social interaction of the conspecifics and, the occurrence of bite wounds[24]. Shifting the coping style towards a more pro-active one has recently been shown to be associated with a lack of CSC-induced colitis and anxiety[10], suggesting this kind of stress coping strategy to promote stress resilience
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