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Focal Increases of Fetal Macrophages in Placentas from Pregnancies with Histological Chorioamnionitis: Potential Role of Fibroblast Monocyte Chemotactic Protein‐1
Author(s) -
Toti Paolo,
Arcuri Felice,
Tang Zhonghua,
Schatz Frederick,
Zambrano Eduardo,
Mor Gil,
NivenFairchild Tracy,
Abrahams Vikki M.,
Krikun Graciela,
Lockwood Charles J.,
Guller Seth
Publication year - 2011
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/j.1600-0897.2010.00927.x
Subject(s) - chorioamnionitis , monocyte , fibroblast , chemotaxis , fetus , placenta , andrology , immunology , macrophage , microbiology and biotechnology , biology , pregnancy , chemistry , medicine , in vitro , receptor , biochemistry , genetics
Citation Toti P, Arcuri F, Tang Z, Schatz F, Zambrano E, Mor G, Niven‐Fairchild T, Abrahams VM, Krikun G, Lockwood CJ, Guller S. Focal increases of fetal macrophages in placentas from pregnancies with histological chorioamnionitis: potential role of fibroblast monocyte chemotactic protein‐1. Am J Reprod Immunol 2011; 65: 470–479 Problem 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. Method of study 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. Conclusion 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.