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 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.