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Social disruption stress exacerbates alpha-galactosylceramide-induced hepatitis in mice

Sonoda, J; Chida, Y; Sudo, N; Kubo, C; (2005) Social disruption stress exacerbates alpha-galactosylceramide-induced hepatitis in mice. NEUROIMMUNOMODULAT , 12 (6) 375 - 379. 10.1159/000091131. Green open access

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Abstract

Objective: Psychosocial stress has been suggested as a possible aggravating factor in liver diseases, however, the underlying mechanism has yet to be clarified. Recently, our research revealed that electric foot-shock stress aggravated NK1.1 Ag+ T cell-dependent a-galactosylceramide (alpha-GalCer)-induced hepatitis in mice via a mechanism mediated by endogenous glucocorticoids. In this study, we examined whether or not such aggravation could be applied to a psychosocially stressful situation, e.g. social disruption stress. Methods: Male wildtype C57BL/6 (B6) or B6 hepatitis virus type B surface antigen transgenic (HBs-tg) mice, a hepatitis B virus carrier mouse model, were exposed 3 times in 1 week to social disruption stress in which an 8-month-old aggressive male intruder was placed into their home cage (5 mice per group) for 2 h. Twelve hours after the final exposure to the stress, the wild-type and HBs-tg mice were intravenously injected with alpha-GalCer. Results:The stress-exposed wild-type mice exhibited significantly reduced thymus weight loss compared with the control animals. Moreover, this stress regimen led to a significant increase in serum alanine aminotransferase levels in both the wild-type and the HBs-tg mice, although the increase in the HBs-tg mice was higher than that in the wild-type mice. Conclusion: These findings demonstrated that, similar to electric foot-shock stress, social disruption stress exacerbated alpha-GalCer-induced hepatitis. Copyright (C) 2005 S. Karger AG, Basel.

Type: Article
Title: Social disruption stress exacerbates alpha-galactosylceramide-induced hepatitis in mice
Open access status: An open access version is available from UCL Discovery
DOI: 10.1159/000091131
Keywords: apoptosis, brain-gut axis, HBs-tg mice, liver injury, psychosocial stress, LARGE ENVELOPE POLYPEPTIDE, T-CELLS, TRANSGENIC MICE, LIVER-INJURY, IMMUNE-RESPONSE, NKT CELLS, APOPTOSIS, RATS, REQUIREMENT, ACTIVATION
UCL classification: UCL
URI: https://discovery.ucl.ac.uk/id/eprint/2929
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