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Abstract
There is convincing evidence from different mouse models that chronic psychosocial stress promotes splenomegaly, basal and lipopolysaccharide (LPS)-induced in vitro splenocyte activation and insensitivity towards glucocorticoids (GC) in in vitro LPS-treated splenocytes. However, we just recently showed, employing the chronic subordinate colony housing (CSC) paradigm, that bite wounds received during stressor exposure drive these stress-induced spleen changes. As skin wounds induced by planned surgery or physical trauma are more adequately reflecting what chronically stressed humans are likely to experience, it was the objective of the present study to investigate whether abdominal surgery prior to stressor exposure also promotes respective stress-induced spleen effects in the absence of any bite wounds. In line with our hypothesis, abdominal surgery prior to CSC induced splenomegaly, increased in vitro cell viability under basal and LPS conditions as well as the delta response to LPS (LPS – basal), and promoted the inability of isolated splenocytes to respond with a decreased cell viability to increasing concentrations of corticosterone following LPS-stimulation in vitro. Together with previous data, these findings demonstrate that physical injury, either in form of received bite wounds during stressor exposure or in form of abdominal surgery prior to stressor exposure, promotes the development of splenic immune activation and GC resistance.
Highlights
There is convincing evidence from different mouse models that chronic psychosocial stress promotes splenomegaly, basal and lipopolysaccharide (LPS)-induced in vitro splenocyte activation and insensitivity towards glucocorticoids (GC) in in vitro LPS-treated splenocytes
The latter is accompanied by increased susceptibility to endotoxic shock[18], which is at least in part due to increased splenic expression of toll-like receptors (TLR)[2] and 419, basal and/or LPS-induced in vitro cell viability[1,10,12] and production of interleukin (IL)-6, IL-1β and tumor necrosis factor (TNF)-α18,20,21, as well as development of GC resistance[1,2,10,12,13,16]
We confirm previous findings[1] by showing that exposure to 19 days of chronic subordinate colony housing (CSC) does not affect spleen size, splenocyteactivity and spleen cell sensitivity to CORT, when significant wounding during stressor exposure is absent. We further extend these findings by showing that abdominal surgery prior to CSC exposure, in line with what we recently reported for bite wounds during CSC exposure[1], promotes splenomegaly, basal and www.nature.com/scientificreports
Summary
There is convincing evidence from different mouse models that chronic psychosocial stress promotes splenomegaly, basal and lipopolysaccharide (LPS)-induced in vitro splenocyte activation and insensitivity towards glucocorticoids (GC) in in vitro LPS-treated splenocytes. If the stressor is of social nature allowing direct physical interaction between the individuals, these circulating CD11b+ cells in a bite wound-dependent manner accumulate in the spleen of socially defeated rodents[1,16,17] The latter is accompanied by increased susceptibility to endotoxic shock[18], which is at least in part due to increased splenic expression of toll-like receptors (TLR)[2] and 419, basal and/or LPS-induced in vitro cell viability[1,10,12] and production of interleukin (IL)-6, IL-1β and tumor necrosis factor (TNF)-α18,20,21, as well as development of GC resistance[1,2,10,12,13,16]. As skin wounds induced by planned surgery or physical trauma are more adequately reflecting what chronically-stressed humans are likely to experience, it was the objective of the present study to investigate whether abdominal surgery prior to stressor exposure promotes stress-induced splenomegaly, spleen cell activation and development of splenic GC resistance in the absence of any bite wounds
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