Regulation of human decidual cell macrophage inflammatory protein-1 alpha (MIP-1 alpha) production by inflammatory cytokines

Abstract

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-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF alpha), and IL-6. Another class of cytokines includes chemokines of the "C-C" subclassification such as macrophage inflammatory protein-1 alpha (MIP-1 alpha). The purpose of this study was to determine whether cultured human decidual cells produce MIP-1 alpha in response to other inflammatory cytokines.

Methods: Various concentrations of IL-1 beta, TNF alpha, IL-6, and IL-4 were incubated with confluent monolayer cultures of decidual cells isolated from normal term placentae for 16 h at 37 degrees C, and MIP-1 alpha concentrations in culture supernatants were measured by ELISA.

Results: We found that incubation of decidual cells with IL-1 beta, TNF alpha, and IL-4 resulted in significant concentration-dependent increases in MIP-1 alpha production. IL-6 had no effect on MIP-1 alpha production.

Conclusions: Our data are the first to show that human decidual cells in culture produce MIP-1 alpha in response to other inflammatory cytokines. We suggest that decidual cell production of MIP-1 alpha is an important early event in the pathophysiology of infection-associated preterm labor.