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Sustained STING-IRF7 signaling aggravates LPS-induced endometrial inflammation via excessive neutrophil extracellular traps generation
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Sustained STING-IRF7 signaling aggravates LPS-induced endometrial inflammation via excessive neutrophil extracellular traps generation
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Journal Article
Sustained STING-IRF7 signaling aggravates LPS-induced endometrial inflammation via excessive neutrophil extracellular traps generation
2026
Overview
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.
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.
We identified neutrophil surface molecular CD11b as a key downstream target of STING, whose expression was transcriptionally regulated via IRF7. Furthermore, the STING-IRF7 axis was found to drive lipocalin-2 (LCN2) expression, which acted through its receptor MC4R to upregulate intracellular adhesion molecule-1 (ICAM-1), thereby facilitating neutrophil recruitment and NETosis during LPS stimulation. The role of this pathway was validated both
using isolated neutrophils and
using
mice. Moreover, STING deficiency reprogramed the endometrial immune microenvironment by reducing inflammatory infiltration and restoring receptivity transcription factor homeobox A10 (HOXA10).
Our findings revealed a novel mechanism in which the STING-IRF7 pathway exacerbated endometrial inflammation and tissue damage by coordinately upregulating CD11b and activating the LCN2-ICAM-1 axis. Consequently, targeting the STING signaling pathway may offer a promising therapeutic strategy for chronic endometritis.
Publisher
Frontiers Media SA,Frontiers Media S.A
Subject
/ Animals
/ CD11b
/ Disease
/ Endometritis - chemically induced
/ Ethics
/ Extracellular Traps - immunology
/ Extracellular Traps - metabolism
/ Female
/ Females
/ Homeobox
/ Intercellular adhesion molecule 1
/ Intercellular Adhesion Molecule-1 - metabolism
/ Interferon regulatory factor 7
/ Interferon Regulatory Factor-7 - genetics
/ Interferon Regulatory Factor-7 - immunology
/ Interferon Regulatory Factor-7 - metabolism
/ IRF7
/ Membrane Proteins - genetics
/ Membrane Proteins - immunology
/ Membrane Proteins - metabolism
/ Mice
/ neutrophil extracellular traps
/ Signal Transduction - immunology
/ STING
