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Regulation of Human Decidual Cell Macrophage Inflammatory Protein‐1α (MIP‐1α) Production by Inflammatory Cytokines
Author(s) -
DUDLEY DONALD J.,
SPENCER SLADE,
EDWIN SAM,
MITCHELL MURRAY D.
Publication year - 1995
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.1600-0897.1995.tb00946.x
Subject(s) - macrophage inflammatory protein , chemokine , decidual cells , tumor necrosis factor alpha , immunology , cytokine , proinflammatory cytokine , biology , inflammation , macrophage , decidua , alpha (finance) , endocrinology , medicine , in vitro , fetus , placenta , pregnancy , biochemistry , genetics , construct validity , nursing , patient satisfaction
PROBLEM : Inflammation of human gestational tissues is a key pathophysiologic event in the genesis of infection‐associated preterm labor. Human gestational tissues produce several inflammatory cytokines after stimulation with bacterial products. These include interleukin‐1β (IL‐1β), tumor necrosis factor‐α (TNFα), and IL‐6. Another class of cytokines includes chemokines of the “C‐C” subclassification such as macrophage inflammatory protein‐1α (MlP‐1α). The purpose of this study was to determine whether cultured human decidual cells produce MIP‐1α in response to other inflammatory cytokines. METHODS : Various concentrations of IL‐1β, TNFα, IL‐6, and IL‐4 were incubated with confluent monolayer cultures of decidual cells isolated from normal term placentae for 16 h at 37°C, and MlP‐1α concentrations in culture supernatants were measured by ELISA. RESULTS : We found that incubation of decidual cells with IL‐1β, TNFα, and IL‐4 resulted in significant concentration‐dependent increases in M1P‐1α production. IL‐6 had no effect on MlP‐1α production. CONCLUSIONS : Our data are the first to show that human decidual cells in culture produce MlP‐1α in response to other inflammatory cytokines. We suggest that decidual cell production of MIP‐1α is an important early event in the pathophysiology of infection‐associated preterm labor.