Maternal regulation of inflammatory cues is required for induction of preterm birth.

JCI Insight
Monica CappellettiSenad Divanovic

Abstract

Infection-driven inflammation in pregnancy is a major cause of spontaneous preterm birth (PTB). Both systemic infection and bacterial ascension through the vagina/cervix to the amniotic cavity are strongly associated with PTB. However, the contribution of maternal or fetal inflammatory responses in the context of systemic or localized models of infection-driven PTB is not well defined. Here, using intraperitoneal or intraamniotic LPS challenge, we examined the necessity and sufficiency of maternal and fetal Toll-like receptor (TLR) 4 signaling in induction of inflammatory vigor and PTB. Both systemic and local LPS challenge promoted induction of inflammatory pathways in uteroplacental tissues and induced PTB. Restriction of TLR4 expression to the maternal compartment was sufficient for induction of LPS-driven PTB in either systemic or intraamniotic challenge models. In contrast, restriction of TLR4 expression to the fetal compartment failed to induce LPS-driven PTB. Vav1-Cre-mediated genetic deletion of TLR4 suggested a critical role for maternal immune cells in inflammation-driven PTB. Further, passive transfer of WT in vitro-derived macrophages and dendritic cells to TLR4-null gravid females was sufficient to induce an inflam...Continue Reading

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Citations

Jul 13, 2021·Frontiers in Immunology·Emily J GregorySing Sing Way
Sep 28, 2021·Frontiers in Cellular and Infection Microbiology·Kwan Young OhJun Sook Park

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Methods Mentioned

BETA
fatty
FCS
ELISA
PCR
light microscopy

Software Mentioned

IVCCA
Prism
FUJIFILM VisualSonics
GraphPad

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