Preterm birth remains the leading cause of perinatal mortality and morbidity, largely as a result of a poor understanding of the precise mechanisms controlling labour onset in humans. Inflammation has long been recognised as a key feature of both preterm and term labour, with an influx of inflammatory cells into the uterus and elevated levels of pro-inflammatory cytokines observed during parturition. Nuclear factor kappa B (NF-kappaB) is a transcription factor family classically associated with inflammation. Accumulating evidence points to a role for NF-kappaB in the physiology and pathophysiology of labour. NF-kappaB activity increases with labour onset and is central to multiple prolabour pathways. Premature or aberrant activation of NF-kappaB may thus contribute to preterm labour. The current understanding of NF-kappaB in the context of human labour is discussed here.
No takes yet. Share an insight, caveat, or question.
Lindström et al. (2005) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: