title: Maternal intravascular inflammation in preterm premature rupture of membranes.
abstract: OBJECTIVE
  Intrauterine inflammation has been implicated in the mechanisms responsible for preterm premature rupture of membranes (PROM). However, it is unclear whether this inflammatory process remains localized to the uterus, at the site of membrane rupture, or extends to the maternal compartment. Flow cytometric analysis is a sensitive method to assess the presence and magnitude of in vivo inflammation. This study was conducted to determine whether preterm PROM is associated with changes in the phenotypic and metabolic characteristics of maternal granulocytes and monocytes consistent with the presence of maternal intravascular inflammation.
  
  
  METHODS
  A prospective cross-sectional study was performed including patients with preterm PROM (n = 43) and normal pregnancy (n = 51). Maternal intravascular inflammation was studied using flow cytometry. Maternal blood was assayed to determine granulocyte and monocyte phenotype using monoclonal antibodies, which included cluster differentiation (CD) markers CD11b, CD14, CD15, CD16, CD18, CD49d, CD62L, CD64, CD66b and human leukocyte antigen (HLA)-DR. The quantities of basal intracellular reactive oxygen species (iROS) and oxidative burst was assessed. Statistical analysis was conducted with the use of non-parametric methods. A p value < 0.01 was considered significant.
  
  
  RESULTS
  Preterm PROM was associated with a significant increase in the median mean channel brightness (MCB) of CD11b, CD14, CD64 and CD66b on granulocytes and median MCB of CD11b on monocytes. The oxidative burst and the stimulation index in both cell types were higher in preterm PROM than in normal pregnancy (p < 0.01).
  
  
  CONCLUSIONS
  Preterm PROM is associated with phenotypic and metabolic changes in circulating granulocytes and monocytes.
authors.affiliation: Perinatology Research Branch, National Institute of Child Health and Human Development, Bethesda, Maryland, USA.
authors.forename: M T
authors.initials: MT
authors.lastname: Gervasi
authors.forename: T
authors.initials: T
authors.lastname: Chaiworapongsa
authors.forename: N
authors.initials: N
authors.lastname: Naccasha
authors.forename: P
authors.initials: P
authors.lastname: Pacora
authors.forename: S
authors.initials: S
authors.lastname: Berman
authors.forename: E
authors.initials: E
authors.lastname: Maymon
authors.forename: J C
authors.initials: JC
authors.lastname: Kim
authors.forename: Y M
authors.initials: YM
authors.lastname: Kim
authors.forename: J
authors.initials: J
authors.lastname: Yoshimatsu
authors.forename: J
authors.initials: J
authors.lastname: Espinoza
authors.forename: R
authors.initials: R
authors.lastname: Romero
mesh_terms: D000293:Adolescent; D000328:Adult; D015415:Biomarkers / Q000097:blood; D003430:Cross-Sectional Studies; D005260:Female; D005322:Premature Rupture of Fetal Membranes / Q000276:immunology*; D005434:Flow Cytometry; D006098:Granulocytes / Q000276:immunology*; D006684:HLA-DR Antigens / Q000276:immunology; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000276:immunology; D009000:Monocytes / Q000276:immunology*; D011247:Pregnancy; D011446:Prospective Studies; D017382:Reactive Oxygen Species / Q000276:immunology; D016897:Respiratory Burst / Q000276:immunology / Q000502:physiology; D014591:Uterine Diseases / Q000097:blood / Q000276:immunology*; D014599:Uterus / Q000382:microbiology
chemical_list: D015415:Biomarkers; D006684:HLA-DR Antigens; D017382:Reactive Oxygen Species