Interleukin-11 induces preterm birth and modulates decidual inflammasome gene expression in mice
Amy Winship, Evdokia Dimitriadis
PLACENTA | W B SAUNDERS CO LTD | Published : 2017
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.
Awarded by NHMRC Australia Project Grant
Awarded by NHMRC Australia Senior Research Fellowship
This work was supported by NHMRC Australia Project Grant (1078674) and the Victorian Government's Operational Infrastructure Support Program. AW was supported by a Cancer Council Victoria Postdoctoral Fellowship. ED was supported by a NHMRC Australia Senior Research Fellowship (550905).