[Stress and embryo implantation].

Spontaneous abortion is the most common adverse pregnancy outcome, and stress has been suggested to be abortogenic in mice and humans. Stress-and/or pregnancy-related hormones (corticotropin releasing hormone, adrenocorticotropin, and progesterone) might interact with peripheral and local immunocompetent cells, such as certain T cell, mast cells or NK cells, and result in changes of cytokine production. In an established murine model, abortions can be triggered by exposing the mice to stress during early gestation. Recent data from this model indicated that increased levels of abortogenic Th1 cytokines, a decrease of progesterone and thus, PIBP were incongruous with successful pregnancy maintenance. Supplementation of progesterone exerts a pregnancy protective effect by induction of a pregnancy-protective Th2 biased immune response. Interestingly, data from a prospective study on human pregnancy revealed that women with a clinically normally progressing pregnancy but low levels of progesterone during the first trimester eventually suffered from a miscarriage. These data indicate that stress may lead to increase abortions by altering the endocrine system, which triggers an immune bias towards an abortogenic cytokine profile. Progesterone may be a good marker to identify a putative thread of a miscarriage in human and progesterone replacement therapy may abrogate this thread by inducing a Th2 biased immune response from the decidua.