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Stress-triggered abortion: inhibition of protective suppression and promotion of tumor necrosis factor-alpha (TNF-alpha) release as a mechanism triggering resorptions in mice.

作者信息

Arck P C, Merali F S, Manuel J, Chaouat G, Clark D A

机构信息

Department of Medicine, McMaster University, Hamilton, Ontario, Canada.

出版信息

Am J Reprod Immunol. 1995 Jan;33(1):74-80. doi: 10.1111/j.1600-0897.1995.tb01141.x.

DOI:10.1111/j.1600-0897.1995.tb01141.x
PMID:7619237
Abstract

PROBLEM

Stress adversely affects pregnancy outcome and has been implicated as an abortogen in both animals and humans. However, the mechanisms whereby stress aborts are largely unknown. Alloimmunization can prevent stress-triggered abortion, and immunization is known to increase transforming growth factor-beta 2 (TGF-beta 2)-related suppressive activity.

METHOD

To investigate these mechanisms, DBA/2J males were mated to CBA/J or C3H/HeJ females, and the pregnant females were exposed to ultrasonic sound stress for a period of 24 h between day 4.5 to 8.5 of pregnancy.

RESULTS

Ultrasonic stress significantly elevated the resorption rate with a peak effect on day 5.5 in the CBA/J females and on day 4.5 in the LPS-resistant C3H/HeJ females. The tumor necrosis factor-alpha (TNF-alpha) release from the decidua was also elevated and the TGF-beta 2-mediated suppressive activity was significantly decreased. The resorption rate only increased when the TNF-alpha/TGF-beta 2 ratio was increased compared to the control.

CONCLUSION

These data suggest that stress may inhibit protective suppressor mechanisms and promote secretion of abortogenic cytokines such as TNF-alpha. Possible mechanisms are discussed.

摘要

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