C/EBPδ deficiency delays infection-induced preterm birth.

ABSTRACT:

Background

Parturition is an inflammation process. Exaggerated inflammatory reactions in infection lead to preterm birth. Although nuclear factor kappa B (NF-κB) has been recognized as a classical transcription factor mediating inflammatory reactions, those mediated by NF-κB per se are relatively short-lived. Therefore, there may be other transcription factors involved to sustain NF-κB-initiated inflammatory reactions in gestational tissues in infection-induced preterm birth.

Methods

Cebpd-deficient mice were generated to investigate the role of CCAAT enhancer-binding protein δ (C/EBPδ) in lipopolysaccharide (LPS)-induced preterm birth, and the contribution of fetal and maternal C/EBPδ was further dissected by transferring Cebpd^-/- or WT embryos to Cebpd^-/-</

SUBMITTER: Lei WJ 

PROVIDER: S-EPMC11462803 | biostudies-literature | 2024 Oct

REPOSITORIES: biostudies-literature