Inflammatory mechanisms of preterm labor and emerging anti-inflammatory interventions.

Preterm birth is a major public health concern, requiring a deeper understanding of its underlying inflammatory mechanisms and to develop effective therapeutic strategies. This review explores the complex interaction between inflammation and preterm labor, highlighting the pivotal role of the dysregulation of inflammation in triggering premature delivery. The immunological environment of pregnancy, characterized by a fragile balance of immune tolerance and resistance, is disrupted in preterm labor, leading to a pathological inflammatory response. Feto-maternal infections, among other pro-inflammatory stimuli, trigger the activation of toll-like receptors and the production of pro-inflammatory mediators, promoting uterine contractility and cervical ripening. Emerging anti-inflammatory therapeutics offer promising approaches for the prevention of preterm birth by targeting key inflammatory pathways. From TLR-4 antagonists to chemokine and interleukin receptor antagonists, these interventions aim to modulate the inflammatory environment and prevent adverse pregnancy outcomes. In conclusion, a comprehensive understanding of the inflammatory mechanisms leading to preterm labor is crucial for the development of targeted interventions in hope of reducing the incidence of preterm birth and improving neonatal health outcomes.
Competing Interests: Declaration of Competing Interest S.C. holds a patent on composition of matter for the use of 101.10/rytvela (IL-1 receptor antagonists, compositions, and methods of treatment, United States patent no. USPTO8618054, May 5, 2005). S.C. and D.M.O. hold a patent on methods for reducing perinatal morbidity and/or mortality (US20210322509, March 9, 2016). The remaining authors have no financial conflicts of interest.
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