STRESS-TRIGGERED ABORTION - INHIBITION OF PROTECTIVE SUPPRESSION AND PROMOTION OF TUMOR NECROSIS FACTOR-ALPHA(TNF-ALPHA) RELEASE AS A MECHANISM TRIGGERING RESORPTIONS IN MICE

PROBLEM: Stress adversely affects pregnancy outcome and has been impli cated as an abortogen in both animals and humans. However, the mechani sms whereby stress aborts are largely unknown. Alloimmunization can pr event stress-triggered abortion, and immunization is known to increase transforming growth factor-beta 2 (TGF-beta 2)-related suppressive ac tivity. METHOD: To investigate these mechanisms, DBA/2J males were mat ed 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 f actor-alpha (TNF-alpha) release from the decidua was also elevated and the TGF-beta 2-mediated suppressive activity was significantly decrea sed. The resorption rate only increased when the TNF-alpha/TGF-beta 2 ratio was increased compared to the control. CONCLUSION: These data su ggest that stress may inhibit protective suppressor mechanisms and pro mote secretion of abortogenic cytokines such as TNF-alpha. Possible me chanisms are discussed.