title: Focal increases of fetal macrophages in placentas from pregnancies with histological chorioamnionitis: potential role of fibroblast monocyte chemotactic protein-1.
abstract: OBJECTIVE
  Histopathological chorioamnionitis (HCA) is caused by microbial-driven infiltration of leukocytes to the maternal-fetal interface resulting in adverse neonatal outcomes in a subset of pregnancies. The role of placental villus macrophages (i.e. Hofbauer cells, HBCs) in the pathophysiology of HCA is unelucidated.
  
  
  METHODS
  The number of HBCs in human term placental villi in HCA and control groups was compared using immunohistochemistry. Levels of monocyte chemotactic protein (MCP-1) expression were measured in primary cultures of syncytioytrophoblasts (SCTs) and fibroblasts (FIBs) treated with bacterial compounds [lipopolysaccharide (LPS) and peptidoglycan] and pro-inflammatory cytokines (TNF-α and IL-1β) using ELISA and quantitative real-time PCR.
  
  
  RESULTS
  Immunohistochemistry revealed a focal increase in HBCs in HCA. Treatment of FIBs with LPS, IL-1β, and TNF-α significantly increased MCP-1 mRNA and protein expression. Conversely, MCP-1 mRNA and protein levels were virtually undetectable in treated and untreated SCTs.
  
  
  CONCLUSIONS
  These results demonstrate cell-type-specific regulation of MCP-1 expression in human placenta. A model is presented in which bacterial products and inflammatory cytokines initiate a fibroblast-driven cytokine cascade resulting in recruitment of fetal monocytes to placenta which focally increases levels of HBCs in pregnancies complicated by HCA.
authors.affiliation: Department of Human Pathology & Oncology-Section of Pathology, University of Siena, Siena, Italy.
authors.forename: Paolo
authors.initials: P
authors.lastname: Toti
authors.forename: Felice
authors.initials: F
authors.lastname: Arcuri
authors.forename: Zhonghua
authors.initials: Z
authors.lastname: Tang
authors.forename: Frederick
authors.initials: F
authors.lastname: Schatz
authors.forename: Eduardo
authors.initials: E
authors.lastname: Zambrano
authors.forename: Gil
authors.initials: G
authors.lastname: Mor
authors.forename: Tracy
authors.initials: T
authors.lastname: Niven-Fairchild
authors.forename: Vikki M
authors.initials: VM
authors.lastname: Abrahams
authors.forename: Graciela
authors.initials: G
authors.lastname: Krikun
authors.forename: Charles J
authors.initials: CJ
authors.lastname: Lockwood
authors.forename: Seth
authors.initials: S
authors.lastname: Guller
mesh_terms: D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000378:metabolism*; D002821:Chorioamnionitis / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology*; D002824:Chorionic Villi / Q000473:pathology; D005260:Female; D005333:Fetus / Q000166:cytology / Q000276:immunology*; D005347:Fibroblasts / Q000166:cytology / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry; D008070:Lipopolysaccharides / Q000276:immunology; D008264:Macrophages / Q000276:immunology*; D010920:Placenta / Q000166:cytology / Q000276:immunology* / Q000473:pathology; D011247:Pregnancy; D011251:Pregnancy Complications, Infectious / Q000276:immunology / Q000473:pathology / Q000503:physiopathology
chemical_list: D018932:Chemokine CCL2; D008070:Lipopolysaccharides