Decidual activation in parturition: examination of amniotic fluid for mediators of the inflammatory response.

The accumulation of bioactive agents (characteristic of an inflammatory-type response) in amniotic fluid is common during term and preterm labor, viz., interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha). In addition, prostaglandins, including PGE2, PGF2 alpha, and PGFM, also accumulate in amniotic fluid in some cases of term and preterm labor. From these observations, a number of critical questions arise. Namely, 1) what is the tissue source of origin of these agents?; 2) what are the stimuli that evoke this inflammatory response?; and, 3) are these bioactive agents of inflammation involved in the commencement of labor or else a natural accompaniment of the parturition process? It is reasonable to suspect that the decidua is activated during parturition as the membranes-decidua are exposed after cervical dilation to the vaginal/cervical secretions. Amnion and chorion laeve, in the human, are avascular tissues that produce PGE2 but not PGF2 alpha. Therefore, the accumulation of PGF2 alpha and PGFM in amniotic fluid during labor cannot be attributed to a fetal membrane origin. Moreover, the fetal membranes and decidua do not convert PGE2 to PGF2 alpha. In addition, the fetal membranes do not produce mature, i.e., secreted 17kD IL-1 beta. On the other hand, the decidua does produce PGF2 alpha and PGFM and is stimulated to do so by agents in the vaginal secretions, namely, bacterial endotoxin and IL-1 beta. After the fetal membranes and contiguous decidua are exposed during the time of cervical dilatation, these tissues are acted upon to cause 1) an influx of mononuclear phagocytes into the forebag compartment of the amniotic fluid; 2) to produce PGF2 alpha and PGFM; and 3) to produce cytokines, including IL-1 beta, IL-6, and TNF-alpha. Exposure of the fetal membranes-decidua to bioactive agents in vaginal/cervical secretions will effect an inflammatory response both in vivo and in vitro. We conclude that the accumulation of bioactive agents characteristic of the inflammatory response in amniotic fluid during term and preterm labor is usually an accompaniment of parturition and not its cause.