Schmidt, Dominic and Reber, Stefan O. and Botteron, Catherine and Barth, Thomas and Peterlik, Daniel and Uschold, Nicole and Maennel, Daniela N. and Lechner, Anja (2010) Chronic psychosocial stress promotes systemic immune activation and the development of inflammatory Th cell responses. BRAIN BEHAVIOR AND IMMUNITY, 24 (7). pp. 1097-1104. ISSN 0889-1591, 1090-2139
Full text not available from this repository. (Request a copy)Abstract
Recent studies indicate that chronic psychosocial stress favors the development of generalized immune dysfunction. During stressor exposure neuroendocrine factors affect numbers and functionality of leukocytes. However, the exact mechanisms leading to systemic changes in immune functions during stress are still not clear. During chronic subordinate colony housing, a model of chronic psychosocial stress, mice developed spontaneous colonic inflammation. Decreased glucocorticoid signaling, induced by a combination of adrenal insufficiency and glucocorticoid resistance, was thought to prevent tempering of local immune cells, and to promote tissue inflammation. In this study we investigated changes in the systemic immune status after chronic subordinate colony housing and analyzed potential mechanisms underlying those alterations. Analysis of T helper cell subsets in peripheral lymph nodes revealed a reduction of regulatory T cells, accompanied by increased T cell effector functions. Generalized activation of T cells was shown by elevated cytokine production upon stimulation. In addition, we observed no apparent shift towards T helper type 2 responses. It is likely, that the previously reported hypocorticism in this stress model led to a steady production of inflammatory Th1, Th2, and Th17 cytokines and obstructed the shift towards an anti-inflammatory response. In conclusion, we established chronic subordinate colony housing as a model to investigate the outcome of stress on the systemic immune status. We also provide evidence that distinct T helper cell subtypes react differentially to the suppressive effect of glucocorticoids. (C) 2010 Elsevier Inc. All rights reserved.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | RHEUMATOID-ARTHRITIS; PSYCHOLOGICAL STRESS; SOCIAL STRESS; TGF-BETA; MICE; COLITIS; T(H)17; MECHANISMS; PARADIGM; DISEASE; Th cell polarization; Th1 cells; Th2 cells; Th17 cells; Chronic psychosocial stress; Glucocorticoids |
| Subjects: | 500 Science > 590 Zoological sciences 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Immunologie Biology, Preclinical Medicine > Institut für Zoologie |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 08 Jul 2020 10:08 |
| Last Modified: | 08 Jul 2020 10:08 |
| URI: | https://pred.uni-regensburg.de/id/eprint/24045 |
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