STRESS-TRIGGERED ABORTION - INHIBITION OF PROTECTIVE SUPPRESSION AND PROMOTION OF TUMOR NECROSIS FACTOR-ALPHA(TNF-ALPHA) RELEASE AS A MECHANISM TRIGGERING RESORPTIONS IN MICE
Pc. Arck et al., STRESS-TRIGGERED ABORTION - INHIBITION OF PROTECTIVE SUPPRESSION AND PROMOTION OF TUMOR NECROSIS FACTOR-ALPHA(TNF-ALPHA) RELEASE AS A MECHANISM TRIGGERING RESORPTIONS IN MICE, American journal of reproductive immunology [1989], 33(1), 1995, pp. 74-80
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.