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DNA From Neutrophil Extracellular Traps Restricts Group 3 Innate Lymphoid Cells Function in Intestinal Epithelial

Bo Xu1,2, Xuezhou Ke1, Xueqian Xie1

  • 1School of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, China.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|June 16, 2026
PubMed
Summary

Neutrophil extracellular traps (NETs) worsen ulcerative colitis (UC) by damaging the intestinal barrier via NET-DNA. This DNA reduces IL-22 production by ILC3s, hindering mucosal repair, but DNase I treatment improves healing.

Keywords:
DNA of neutrophil extracellular trapscoiled‐coil domain containing protein 25group 3 innate lymphoid cellsintestinal mucosal barrierulcerative colitis

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Area of Science:

  • Gastroenterology
  • Immunology
  • Molecular Biology

Background:

  • Neutrophil extracellular traps (NETs) accumulate in ulcerative colitis (UC), impairing intestinal barrier integrity.
  • The precise mechanisms by which NETs impact intestinal epithelial repair in UC remain largely unknown.

Purpose of the Study:

  • To elucidate the molecular mechanisms linking excess NETs to intestinal epithelial damage in UC mouse models.
  • To investigate the role of NET-derived cell-free DNA (NET-DNA) in UC pathogenesis and mucosal healing.

Main Methods:

  • Comparison of wild-type and PAD4 knockout mice, RNA-sequencing for gene expression analysis (IL-22 mRNA).
  • Flow cytometry to assess IL-22 secretion by group 3 innate lymphoid cells (ILC3s) and other DNA forms' effects.
  • In vitro studies using lymphocyte cell lines (MNK3) and intestinal epithelial cells (Caco-2) to evaluate NET-DNA's impact on barrier function and IL-22 regulation via CCDC25 and ILK-HIF-1α pathways.

Main Results:

  • UC mice exhibited elevated NET-DNA, correlating with worsened UC symptoms; DNase I treatment ameliorated these symptoms.
  • NET-DNA specifically reduced IL-22 secretion by ILC3s, mediated through the CCDC25 receptor, impacting IL-22+ILC3s ratio.
  • NET-DNA exposure in vitro impaired intestinal epithelial barrier integrity (increased permeability, reduced ZO-1 expression) and decreased IL-22 levels, while inhibiting ILK-HIF-1α restored IL-22 production.

Conclusions:

  • NET-DNA contributes to UC pathogenesis by suppressing IL-22 production from ILC3s via CCDC25, thereby hindering mucosal healing.
  • Targeting NETs or their DNA components may represent a therapeutic strategy for promoting intestinal barrier repair in UC.