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. [Display omitted] • Preterm labor pathways are initiated and maintained by inflammation. • Inhibiting the inflammatory response associated to preterm labor with emerging anti-inflammatory therapeutics shows promise in preventing preterm birth. • The collaboration between regulatory institutions, clinicians, advocates, and researchers is necessary to bring awareness to this unmet medical need and to develop effective therapeutics destined to prevent preterm birth. [ABSTRACT FROM AUTHOR]