The increase in IL-6 production by fetal membranes in response to infection is likely a non-specific innate response and not an indicator of a functional mediator of any labor-inducing pathways.
This may suggest that other biochemical pathways to labor and parturition are activated at advanced gestational age.
Across the differing conditions of altitude and labor, three primary metabolic pathways (energy, oxidative stress, and protein metabolism) are consistently affected and appear to play a role in placental adaptation to chronic hypoxia.
In the timed pregnant rat model, we have shown that as labor begins, an ERK pathway is activated that phosphorylates CaD [10] and removes the inhibitory influences of CaD on actomyosin interactions [15] and, as a result contributes to the onset of labor [7].
It has been hypothesized that both preterm and term labor share this common pathway and that pathological stimuli of parturition, as described in the following sections, may act in concert with the normal physiological preparation for labor, especially after 32 weeks of gestation.
Surges of stress hormones during labor progress development of essential pathways that will enable the infant to survive outside the womb, thus implicating changes in the genome in response to stress.
MicroRNAs (miRNAs) play a modulatory role in pathways that lead to labor onset, although oxytocin is known to modulate gene expression within the myometrium.
Untimely activation of these inflammatory pathways leads to preterm labor, which can result in preterm birth.
The up-regulated immune-related pathways in the preterm labor group (group AC) placentas further indicated that immunoreaction was one of the important risk factors in preterm labor.
However, information about differences in the amniotic fluid proteome at the end of labor, when activation of prolabor inflammatory pathways may diminish the response to infection, is lacking.
