The complex mechanisms controlling human parturition involves mother, fetus, and placenta, and stress is a key element activating a series of physiological adaptive responses. Preterm birth is a clinical syndrome that shares several characteristics with term birth. A major role for the neuroendocrine mechanisms has been proposed, and placenta/membranes are sources for neurohormones and peptides. Oxytocin (OT) is the neurohormone whose major target is uterine contractility and placenta represents a novel source that contributes to the mechanisms of parturition. The CRH/urocortin (Ucn) family is another important neuroendocrine pathway involved in term and preterm birth. The CRH/Ucn family consists of four ligands: CRH, Ucn, Ucn2, and Ucn3. These peptides have a pleyotropic function and are expressed by human placenta and fetal membranes. Uterine contractility, blood vessel tone, and immune function are influenced by CRH/Ucns during pregnancy and undergo major changes at parturition. Among the others, neurohormones, relaxin, parathyroid hormone-related protein, opioids, neurosteroids, and monoamines are expressed and secreted from placental tissues at parturition. Preterm birth is the consequence of a premature and sustained activation of endocrine and immune responses. A preterm birth evidence for a premature activation of OT secretion as well as increased maternal plasma CRH levels suggests a pathogenic role of these neurohormones. A decrease of maternal serum CRH-binding protein is a concurrent event. At midgestation, placental hypersecretion of CRH or Ucn has been proposed as a predictive marker of subsequent preterm delivery. While placenta represents the major source for CRH, fetus abundantly secretes Ucn and adrenal dehydroepiandrosterone in women with preterm birth. The relevant role of neuroendocrine mechanisms in preterm birth is sustained by basic and clinic implications.

Neuroendocrine Mechanisms in Pregnancy and Parturition

Effects of relaxation on psychobiological wellbeing during pregnancy: a randomized controlled trial.

Background and aims: Psychological stress plays an important role in an array of intestinal disorders. Corticotrophin releasing hormone (CRH) is involved in the pathogenic process induced by psychological stress. The peripheral sources of CRH remain to be further understood. This paper aims to identify the sources of CRH in the intestine. Methods and results: Mice were treated with chronic restraint stress. A double-labelling approach was taken to localise CRH expression in immune cells (including dendritic cells, mast cells, lymphocytes, enterochromaffin cells and eosinophils) in the intestine by confocal microscopy and flow cytometry. As CRH was identified in eosinophils, a cell line of eosinophil, EoL-1 cells were treated with an array of putative stress mediators. The results showed that substance P (SP) induced the expression/release of CRH in eosinophils via neurokinin receptor 1 and 2. Co-culturing SP-primed eosinophils with the mast cell line, HMC-1 cells, we found that HMC-1 cells were activated by eosinophil-derived CRH that further induced T84 monolayer barrier dysfunction, which was further confirmed by a mouse model study. Conclusion: Eosinophils express CRH in the jejunum in response to psychological stress. SP and its receptors mediate the effect of stress in the CRH expression in eosinophils. Eosinophil-derived CRH activates mast cells to induce the jejunum epithelial barrier dysfunction.

https://gut.bmj.com/content/gutjnl/58/11/1473.full.pdf

Psychological stress induces eosinophils to produce corticotrophin releasing hormone in the intestine.

Mast cell activation and autism

Intimate partner violence, substance use, and adverse neonatal outcomes among urban women.

Maternal serum corticotropin-releasing hormone and ACTH levels as predictive markers of premature labor

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Maternal serum corticotropin-releasing hormone and ACTH levels as predictive markers of premature labor