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.