Neutrophil-Fibroblast Crosstalk Drives Immunofibrosis in Sequelae of Pelvic Inflammatory Disease Through Neutrophil Extracellular Traps.

ABSTRACT:

Background

Due to the complex pathogenesis of sequelae of pelvic inflammatory disease (SPID), targeted therapeutic agents are still lacking. Here, we investigated the interactions between neutrophils and uterine fibroblasts (FBs) in developing tissue fibrosis in SPID.

Methods

A rat model of SPID was constructed to assess the roles of autophagy and neutrophil extracellular traps (NETs) in SPID rats. Single-cell sequencing data from the public database GSE223639 were utilized to identify the specific cell cluster FBs where NETs act. A DMSO-induced HL-60-driven neutrophil-like (dHL-60) cell model was established, and neutrophil-like cells were treated with rapamycin and MHY1485 to activate and inhibit autophagy, respectively, to observe the differences in the production of NETs

SUBMITTER: Dang C 

PROVIDER: S-EPMC12626693 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature