Animal Models of Chorioamnionitis: Considerations for Translational Medicine

Abstract

Preterm birth is defined as any birth occurring before 37 completed weeks of gestation by the World Health Organization. Preterm birth is responsible for perinatal mortality and long-term neurological morbidity. Acute chorioamnionitis is observed in 70% of premature labor and is associated with a heavy burden of multiorgan morbidities in the offspring. Unfortunately, chorioamnionitis is still missing effective biomarkers and early placento- as well as feto-protective and curative treatments. This review summarizes recent advances in the understanding of the underlying mechanisms of chorioamnionitis and subsequent impacts on the pregnancy outcome, both during and beyond gestation. This review also describes relevant and current animal models of chorioamnionitis used to decipher associated mechanisms and develop much needed therapies. Improved knowledge of the pathophysiological mechanisms underpinning chorioamnionitis based on preclinical models is a mandatory step to identify early in utero diagnostic biomarkers and design novel anti-inflammatory interventions to improve both maternal and fetal outcomes.

Keywords: animal models; chorioamnionitis; preterm birth.

Figure 1

Physiopathology of CA at the maternal and fetal sides. Maternal inflammatory response is defined as stage 1 in case of acute subchorionitis or chorionitis, stage 2 in case of acute CA: polymorphonuclear leukocytes extend into fibrous chorion or, amnion and stage 3 in case of necrotizing CA: karyorrhexis of polymorphonuclear leukocytes, amniocyte necrosis, and/or amnion basement membrane hypereosinophilia. Fetal inflammatory response is defined as stage 1 in the case of chorionic vasculitis or umbilical phlebitis, stage 2 in case of involvement of the umbilical vein and one or more umbilical arteries, and stage 3 in case of necrotizing funisitis [1]. (Created with BioRender.com 23 March 2022).