Abstract

Preterm birth before 32 weeks' gestation is the leading cause of perinatal morbidity and mortality; the incidence appears to be rising and interventions to reduce the trend are urgently needed (Anonymous, 2006). Inflammation appears to be the final common pathway to preterm birth, causing uterine contractions, cervical ripening and rupture of the membranes; increased levels of pro-inflammatory cytokines are found in the myometrium, membranes and amniotic fluid of women in preterm labour and there is an associated influx of inflammatory cells into the uterus (Lindström and Bennett, 2005).

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