Abstract

Background: Preterm birth (PTB) is a major cause of neonatal mortality and morbidity. Intrauterine inflammation (IUI) or chorioamnionitis is considered to promote PTB. There is no effective therapy for treating IUI or PTB. Moreover, clinically relevant mechanisms that initiate and propagate IUI remain a fundamental knowledge gap to develop better therapies. Thus, there is a clear need for defining the mechanism for IUI. Activation of IL-1 receptor-associated kinase 1 (IRAK1) is central in engaging immune signaling pathways, including NFkB and MAP …

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