Preterm labor is a worldwide public health problem, representing the first cause of neonatal morbimortality. Experimental and clinical evidences strongly suggest that preterm labor, as well as normal (term) labor, are the result of an inflammatory process that is mediated by maternal leukocytes. These immune cells are primed in peripheral blood and then infiltrate the maternal-fetal interface where they modulate the local mechanical and biochemical signaling that results in uterine contractions, cervical dilation and ripening and rupture of the fetal membranes.
After many decades of research, several factors have been associated with the development of preterm labor, yet current strategies aimed at its prediction and prevention have proven to be mainly ineffective, since its prevalence has not been reduced. Such research and strategies have been congruent with the dominating medical and scientific materialistic paradigm which presupposes that only material causes can produce material effects. From this view, the etiology of a phenomenon such as preterm labor must be fundamentally of biochemical nature and the pregnant woman that develops the condition has very little influence over it, if any.
However, the problem of preterm labor could be considered from a different paradigm, one centered in the person and more holistic in the sense that it considers that non-material (i.e. mental) phenomena may causally influence over material physiological processes (e.g. cellular functions, gene and protein expression). In this sense, recent evidences show an association between the psychosocial stress that is perceived by the pregnant woman and the development of preterm labor. However, the cellular and molecular mechanisms mediating such relation are yet to be elucidated.
It is well known that perceived stress can influence the immune function by way of the neuroendocrine mediators produced by the activation of the hypothalamic-pituitary-adrenal axis, including cortisol, adrenaline and corticotropin releasing hormone. These molecules have the capacity not only of activating leukocytes but also of altering the production of other hormones critical to the normal development of pregnancy, such as progesterone and prolactin.
We hypothesize that high levels of psychosocial stress in the pregnant woman would be associated with an increase in circulating neuroendocrine mediators, corresponding to an increase in their receptors in maternal peripheral leukocytes. This would lead to leukocyte activation and increased expression of inflammatory cytokines, which would correlate to an increased incidence of preterm labor.