Interleukin-11 induces preterm birth and modulates decidual inflammasome gene expression in mice

Abstract

Decidual inflammation and inflammasome activation contribute to the pathogenesis of preterm birth (PTB). Interleukin-(IL)11 exerts complex regulatory effects on inflammation and IL-11 protein is elevated in PTB decidua. We aimed to determine a functional role for IL-11 in parturition or PTB. IL-11 administration during middle-late gestation pregnancy induced preterm birth in 87.5% of mice versus saline controls. Litters from IL-11-treated mothers had reduced offspring weight and numbers of live pups. IL-11 up-regulated decidual gene expression of key components of the inflammasome including IL-1β, Caspase-1 and ASC. This is the first report of a causal role for IL-11 in PTB in vivo.