Foertsch, Sandra and Fuechsl, Andrea M. and Faller, Sandra D. and Hoelzer, Hannah and Langgartner, Dominik and Messmann, Joanna and Strauss, Gudrun and Reber, Stefan O. (2017) Splenic glucocorticoid resistance following psychosocial stress requires physical injury. SCIENTIFIC REPORTS, 7: 15730. ISSN 2045-2322,
Full text not available from this repository. (Request a copy)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 reactive coping style.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | REPEATED SOCIAL DEFEAT; MALE-MICE; MOLECULAR-MECHANISMS; IN-VITRO; HPA-AXIS; INFLAMMATION; RESILIENCE; ANXIETY; RATS; SUSCEPTIBILITY; |
| Subjects: | 500 Science > 530 Physics |
| Divisions: | Biology, Preclinical Medicine > Institut für Physiologie |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 14 Dec 2018 13:19 |
| Last Modified: | 25 Feb 2019 14:56 |
| URI: | https://pred.uni-regensburg.de/id/eprint/1843 |
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