Michal A Elovitz1, Juan Gonzalez. 1. Center for Research in Reproduction and Women's Health, Department of Obstetrics & Gynecology, University of Pennsylvania, Philadelphia, Pennsylvania, USA. melovitz@obgyn.upenn.edu
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.
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.
Authors: Roberto Romero; Shali Mazaki-Tovi; Edi Vaisbuch; Juan Pedro Kusanovic; Tinnakorn Chaiworapongsa; Ricardo Gomez; Jyh Kae Nien; Bo Hyun Yoon; Moshe Mazor; Jingqin Luo; David Banks; John Ryals; Chris Beecher Journal: J Matern Fetal Neonatal Med Date: 2010-05-26
Authors: Irina Burd; Amy I Bentz; Jinghua Chai; Juan Gonzalez; Hubert Monnerie; Peter D Le Roux; Akiva S Cohen; Marc Yudkoff; Michal A Elovitz Journal: J Neurosci Res Date: 2010-07 Impact factor: 4.164
Authors: Michal A Elovitz; Amy G Brown; Kelsey Breen; Lauren Anton; Monique Maubert; Irina Burd Journal: Int J Dev Neurosci Date: 2011-03-04 Impact factor: 2.457
Authors: Sonia S Hassan; Roberto Romero; Adi L Tarca; Chia-Ling Nhan-Chang; Edi Vaisbuch; Offer Erez; Pooja Mittal; Juan Pedro Kusanovic; Shali Mazaki-Tovi; Lami Yeo; Sorin Draghici; Jung-Sun Kim; Niels Uldbjerg; Chong Jai Kim Journal: J Matern Fetal Neonatal Med Date: 2009-12
Authors: Brianna Lyttle; Jinghua Chai; Juan M Gonzalez; Hua Xu; Mary Sammel; Michal A Elovitz Journal: Am J Obstet Gynecol Date: 2009-09 Impact factor: 8.661
Authors: Irina Burd; Jinghua Chai; Juan Gonzalez; Ella Ofori; Hubert Monnerie; Peter D Le Roux; Michal A Elovitz Journal: Am J Obstet Gynecol Date: 2009-09 Impact factor: 8.661