Sustained STING-IRF7 signaling aggravates LPS-induced endometrial inflammation via excessive neutrophil extracellular traps generation.

ABSTRACT:

Introduction

The stimulator of interferon genes (STING) is a central mediator of innate immune sensing and represents a critical regulator of chronic inflammation. Upon persistent infection, excessive neutrophil activation leads to the formation of neutrophil extracellular traps (NETs) that damage the tissues. However, the mechanism by which STING signaling regulates NETs formation under chronic inflammatory conditions remains poorly understood.

Methods

In this study, using LPS-induced murine endometritis models in wild-type and STING-deficient mice, we demonstrated that STING deficiency significantly suppressed myeloperoxidase activity, and diminished NETs formation.

Results

We identified neutrophil surface molecular CD11b as a key downstream target of STING, whose e

SUBMITTER: Chu M 

PROVIDER: S-EPMC12827698 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature