Conclusion
Pro-inflammatory mediators play a central role in the pathophysiology of preterm labour and may constitute the main targets for therapeutic interventions in the prevention and clinical management of preterm labour. Imbalances in the pro- and anti-inflammatory pathways maybe responsible for preterm labour and postterm pregnancies respectively. Increased expression of pro-inflammatory mediators such as IL-1β, IL-6, IL-8 and TNF-α are associated with increased risk of preterm birth. Although the etiology of preterm labour remains elusive, alteration in multiple maternal and foetal physiological mechanisms are implicated including genetic predisposition, psychological and environmental influences.
Available medical therapies for preterm labour have not been consistently effective in aborting uterine contractions due to its ill-defined pathophysiology. However, therapeutic interventions primarily targeting the pro-inflammatory pathway seem promising as inflammation plays a central role in the pathogenesis. In-depth understanding of the mechanistic role of proinflammatory mediators remains vital to the development of more efficacious therapies and interventions for prevention and treatment of preterm labour. Further research of high methodological quality is recommended to provide adequate understanding of the pathophysiological mechanisms of maternal pro-inflammatory mediators in preterm labour.