Lloyd, J; (2006) The role of inflammation in preterm labour and perinatal outcome. Doctoral thesis , UCL (University College London).

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Abstract

There is evidence pointing towards materno-fetal inflammatory pathways with release of pro inflammatory cytokines as being key to the initiation of preterm labour. However the direct relationship between inflammation and neonatal outcome remains unclear, as histological chorioamnionitis is relatively common in pregnancies that deliver prematurely but significant white matter injury is only seen in a minority of these infants. Expression of the major histocompatibility complex type II (MHC Class II) on the surface of circulating monocytes has been used as a measure of cytokine balance, as it is partly regulated by cytokines and levels of surface expression are decreased by the anti-inflammatory cytokine, interleukin 10 (IL-10). The work presented here examines the hypothesis that monocyte MHC Class II expression is lower in preterm labour, reflecting an anti-inflammatory response, and that the severity of inflammatory challenge may correlate with perinatal morbidity and mortality. Blood was taken from women in labour at term (n=29), undergoing elective caesarean section (n=23), in preterm labour (PTL) (n=14) or with preterm prelabour rupture of membranes (PPROM) (n=24) at <32 weeks, and a pregnant comparator group of equivalent gestational age (n=57). Blood was also taken from the umbilical cord of infants born following term labour (n=26), term elective caesarean section (n=24), feticides (n=7), PTL (n=16), PPROM (n=9) and caesarean section at <32 weeks for IUGR (n=13). Monocyte MHC Class II expression and plasma cytokine levels of TNFa, FJL-ip, IL-6, IL-8, IL-10 and EL-12 were measured using flow cytometry. Plasma levels of TGFPi were assayed using an ELISA. Cytokine production by whole blood in response to E. Coli lipopolysaccharide (LPS) was quantified at 24 hours.

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