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

Junko Sonoda, Yoichi Chida, Nobuyuki Sudo, Chiharu Kubo

研究成果: ジャーナルへの寄稿学術誌査読

7 被引用数 (Scopus)

抄録

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 α-galactosylceramide (α-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 wild-type 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 α-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 α-GalCer-induced hepatitis.

本文言語英語
ページ(範囲)375-379
ページ数5
ジャーナルNeuroImmunoModulation
12
6
DOI
出版ステータス出版済み - 3月 2006

!!!All Science Journal Classification (ASJC) codes

  • 免疫学
  • 内分泌学
  • 神経学
  • 内分泌系および自律システム

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