title: Human labour is associated with a decline in myometrial chemokine receptor expression: the role of prostaglandins, oxytocin and cytokines.
abstract: OBJECTIVE
  Human labour is an inflammatory process with a heavy infiltration of immune cells into the myometrium and cervix induced by local chemokine production. Myometrial cells also express chemokine receptors, but there is little information about their behaviour or function during pregnancy and labour.
  
  
  METHODS
  We studied the behaviour of the receptors (CCR2, CXCR1 and CXCR2) for the CCL2 and CXCL8 in human myometrium, because both have been shown to be important in labour.
  
  
  RESULTS
  We found that there was a significant decline in the mRNA expression of all three receptors in the upper segment and a similar trend in the lower segment with the onset of term labour (TL). Chemokine receptor mRNA expression was increased by stretch, reduced by oxytocin and PGF(2α)  acting via phospholipase C (PLC). CXCR2 declined with exposure to CXCL8, consistent with the negative relationship observed in labouring myometrial tissue. The mRNA changes were confirmed by western analysis and flow cytometry.
  
  
  CONCLUSIONS
  These data show that myometrial chemokine receptor expression is reduced with the onset of term labour probably in response to the increased activity of chemokines, oxytocin and PGF(2α) .
authors.affiliation: Imperial College Parturition Research Group, Academic Department of Obstetrics & Gynaecology, Imperial College School of Medicine, Chelsea and Westminster Hospital, London, UK.
authors.forename: Renyi
authors.initials: R
authors.lastname: Hua
authors.forename: James E
authors.initials: JE
authors.lastname: Pease
authors.forename: Weiwei
authors.initials: W
authors.lastname: Cheng
authors.forename: Suren R
authors.initials: SR
authors.lastname: Sooranna
authors.forename: Jonathan M
authors.initials: JM
authors.lastname: Viney
authors.forename: Scott M
authors.initials: SM
authors.lastname: Nelson
authors.forename: Les
authors.initials: L
authors.lastname: Myatt
authors.forename: Philip R
authors.initials: PR
authors.lastname: Bennett
authors.forename: Mark R
authors.initials: MR
authors.lastname: Johnson
mesh_terms: D002478:Cells, Cultured; D016207:Cytokines / Q000494:pharmacology / Q000502:physiology*; D015237:Dinoprost / Q000494:pharmacology / Q000502:physiology; D015232:Dinoprostone / Q000494:pharmacology / Q000502:physiology; D015536:Down-Regulation; D005260:Female; D006801:Humans; D007743:Labor, Obstetric / Q000187:drug effects* / Q000276:immunology; D040542:Mechanotransduction, Cellular; D009215:Myometrium / Q000187:drug effects / Q000276:immunology*; D007752:Obstetric Labor, Premature / Q000276:immunology; D010121:Oxytocin / Q000494:pharmacology / Q000502:physiology*; D011247:Pregnancy; D011453:Prostaglandins / Q000494:pharmacology / Q000502:physiology*; D054390:Receptors, CCR2 / Q000096:biosynthesis* / Q000235:genetics; D023062:Receptors, Interleukin-8A / Q000096:biosynthesis* / Q000235:genetics; D023063:Receptors, Interleukin-8B / Q000096:biosynthesis* / Q000235:genetics
chemical_list: C515334:CCR2 protein, human; D016207:Cytokines; D011453:Prostaglandins; D054390:Receptors, CCR2; D023062:Receptors, Interleukin-8A; D023063:Receptors, Interleukin-8B; D010121:Oxytocin; D015237:Dinoprost; D015232:Dinoprostone