| Autor: |
Boeckel SRV; Tommy's Centre for Maternal and Fetal Health at the MRC Centre for Reproductive Health, University of Edinburgh, QMRI, Edinburgh, United Kingdom., Hrabalkova L; Tommy's Centre for Maternal and Fetal Health at the MRC Centre for Reproductive Health, University of Edinburgh, QMRI, Edinburgh, United Kingdom., Baker TL; University of Edinburgh Centre for Inflammation Research, QMRI, Edinburgh, United Kingdom., MacPherson H; Tommy's Centre for Maternal and Fetal Health at the MRC Centre for Reproductive Health, University of Edinburgh, QMRI, Edinburgh, United Kingdom., Frew L; Tommy's Centre for Maternal and Fetal Health at the MRC Centre for Reproductive Health, University of Edinburgh, QMRI, Edinburgh, United Kingdom., Boyle AK; Tommy's Centre for Maternal and Fetal Health at the MRC Centre for Reproductive Health, University of Edinburgh, QMRI, Edinburgh, United Kingdom., McHugh BJ; University of Edinburgh Centre for Inflammation Research, QMRI, Edinburgh, United Kingdom., Wilson K; Tommy's Centre for Maternal and Fetal Health at the MRC Centre for Reproductive Health, University of Edinburgh, QMRI, Edinburgh, United Kingdom., Norman JE; Tommy's Centre for Maternal and Fetal Health at the MRC Centre for Reproductive Health, University of Edinburgh, QMRI, Edinburgh, United Kingdom., Dorin JR; University of Edinburgh Centre for Inflammation Research, QMRI, Edinburgh, United Kingdom., Davidson DJ; University of Edinburgh Centre for Inflammation Research, QMRI, Edinburgh, United Kingdom., Stock SJ; Tommy's Centre for Maternal and Fetal Health at the MRC Centre for Reproductive Health, University of Edinburgh, QMRI, Edinburgh, United Kingdom. Sarah.Stock@ed.ac.uk. |
| Abstrakt: |
Preterm birth, defined as delivery before 37 weeks of gestation, is the leading cause of neonatal mortality and morbidity. Infection and inflammation are frequent antecedents of spontaneous preterm birth. Cathelicidin, an antimicrobial host defence peptide, is induced by infection and inflammation and although expressed in the reproductive tract and fetal tissues, its role in the pathogenesis of spontaneous preterm birth is unknown. Here we demonstrate that cathelicidin expression is increased at RNA and protein level in the mouse uterus in a model of inflammation-induced labour, where ultrasound guided intrauterine injection of lipopolysaccharide (LPS) at E17 stimulates preterm delivery within 24 hours. Cathelicidin-deficient (Camp -/- ) mice are less susceptible to preterm delivery than wild type mice following intrauterine injection of 1 μg of LPS, and this is accompanied by a decrease in circulating IL-6, an inflammatory mediator implicated in the onset of labour. We also show that the proportion of cathelicidin expressing cells in the myometrium is higher in samples obtained from women in labour at term than pre-labour. Together, these data suggest that cathelicidin has roles in mediating pro-inflammatory responses in a murine model of inflammation-induced labour, and in human term labour. |
