title: Phenotypic and metabolic characteristics of maternal monocytes and granulocytes in preterm labor with intact membranes.
abstract: OBJECTIVE
  Experimental and clinical studies support a role for the fetus in the control of the onset of labor. Fetal systemic inflammation, but not a maternal inflammatory response, has been linked to the onset of preterm labor and delivery on the basis of the determination of inflammatory cytokines in fetal and maternal blood. We propose that parturition requires fetomaternal cooperation and that inflammation is an integral part of the parturitional process. This study used flow cytometry, a sensitive technique for the detection of intravascular inflammation, to assess whether maternal inflammation is present in preterm labor.
  
  
  METHODS
  A prospective cross-sectional study was performed including patients with preterm labor (n = 55) and women with normal pregnancy (n = 50). Intravascular inflammation was studied by using flow cytometry. Maternal blood was assayed to determine granulocyte and monocyte phenotype by using monoclonal antibodies, which included the following cluster of differentiation (CD) markers: CD11b, CD14, CD15, CD16, CD18, CD49d, CD62L, CD64, CD66b, and HLA-DR. Oxidative burst and generation of basal intracellular oxygen radical species were assessed. Statistical analysis was conducted with the use of nonparametric methods. A P value of <.01 was considered statistically significant.
  
  
  RESULTS
  Preterm labor was associated with a significant increase in the median mean channel brightness of CD11b, CD15, and CD66b on granulocytes and median mean channel brightness of CD11b and CD15 on monocytes. The ratio of oxidative burst over basal intracellular oxygen radical species in both granulocytes and monocytes was increased in preterm labor (P <. 01).
  
  
  CONCLUSIONS
  Preterm labor with intact membranes is associated with phenotypic and metabolic changes of maternal granulocytes and monocytes.
authors.affiliation: Perinatology Research Branch, National Institute of Child Health and Human Development, Bethesda, Md, 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: S
authors.initials: S
authors.lastname: Blackwell
authors.forename: B H
authors.initials: BH
authors.lastname: Yoon
authors.forename: E
authors.initials: E
authors.lastname: Maymon
authors.forename: R
authors.initials: R
authors.lastname: Romero
mesh_terms: D000328:Adult; D015703:Antigens, CD; D000951:Antigens, Neoplasm; D015815:Cell Adhesion Molecules; D003430:Cross-Sectional Studies; D005321:Extraembryonic Membranes / Q000503:physiopathology*; D005260:Female; D058851:GPI-Linked Proteins; D006098:Granulocytes / Q000502:physiology*; D006801:Humans; D016256:Lewis X Antigen / Q000032:analysis; D016177:Macrophage-1 Antigen / Q000032:analysis; D008562:Membrane Glycoproteins / Q000032:analysis; D009000:Monocytes / Q000502:physiology*; D007752:Obstetric Labor, Premature / Q000097:blood* / Q000503:physiopathology*; D010641:Phenotype; D011247:Pregnancy / Q000097:blood*; D011446:Prospective Studies; D017382:Reactive Oxygen Species / Q000097:blood; D012016:Reference Values; D016897:Respiratory Burst
chemical_list: D015703:Antigens, CD; D000951:Antigens, Neoplasm; C504120:CEACAM8 protein, human; D015815:Cell Adhesion Molecules; D058851:GPI-Linked Proteins; D016256:Lewis X Antigen; D016177:Macrophage-1 Antigen; D008562:Membrane Glycoproteins; D017382:Reactive Oxygen Species