Medroxyprogesterone acetate modulates the immune response in the uterus, cervix and placenta in a mouse model of preterm birth.

Abstract

OBJECTIVE: These studies sought to determine whether a progestational agent, specifically medroxyprogesterone acetate (MPA) prevents inflammation-induced preterm birth, in a mouse model, through modulation of the host immune response. STUDY DESIGN: Using an established mouse model of inflammation-induced preterm birth, the activation of the immune response in maternal serum, uterus, cervix and placenta was assessed. In addition, the ability of MPA to modulate this response was investigated. Message RNA and protein expression were assessed by quantitative PCR and ELISAs respectively. RESULTS: Intrauterine inflammation promotes a significant up-regulation of both TH1 and TH2 mediators in all tissues studies though the response is divergent by time and tissue studied. MPA significantly differentially regulates this immune response in the uterus, cervix and placenta. CONCLUSIONS: In the setting of inflammation-induced preterm birth, the host immune response is activated and not limited to a traditional TH1 bias. The ability of MPA to modulate the immune response may be a critical mechanism by which progestins prevent preterm birth.