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Irf5 deficiency in myeloid cells prevents necrotizing enterocolitis by inhibiting M1 macrophage polarization

Jia Wei1, Daxing Tang1, Chengjie Lu1

  • 1Children's Hospital, Zhejiang University School of Medicine, Hangzhou, China.

Mucosal Immunology
|May 16, 2019
PubMed

Insights

Interferon regulatory factor 5 (IRF5) drives necrotizing enterocolitis (NEC) by promoting M1 macrophage polarization. Deleting IRF5 in myeloid cells prevents NEC, offering a potential therapeutic target for this devastating newborn disease.

Area of Science:

  • Neonatal immunology
  • Gastrointestinal disease mechanisms
  • Inflammatory pathways

Background:

  • Necrotizing enterocolitis (NEC) is a critical neonatal inflammatory condition with unclear pathogenesis.
  • Interferon regulatory factor 5 (IRF5) regulates macrophage function and M1 polarization, which are implicated in NEC.
  • Previous research suggests M1 macrophages contribute to NEC injury.

Purpose of the Study:

  • To investigate the role of IRF5 in the pathogenesis of NEC.
  • To determine if IRF5 influences macrophage polarization in NEC.
  • To evaluate the therapeutic potential of targeting IRF5 in myeloid cells for NEC prevention.

Main Methods:

  • Analysis of IRF5 expression in human and murine NEC models.
  • Assessment of macrophage polarization (M1/M2 phenotypes) in NEC.
  • Generation of myeloid-specific Irf5-deficient mice for experimental NEC studies.
  • Evaluation of intestinal epithelial cell apoptosis and barrier function.
  • Bioinformatic and chromatin immunoprecipitation assays to identify IRF5 target genes.

Main Results:

  • IRF5 was upregulated in macrophages from neonates with NEC and in experimental murine NEC.
  • Macrophages in experimental NEC were predominantly M1 polarized.
  • Myeloid-specific deletion of Irf5 significantly reduced M1 polarization, systemic inflammation, and prevented experimental NEC.
  • Ablation of Irf5 suppressed intestinal epithelial cell apoptosis and improved intestinal barrier function.
  • IRF5 was found to bind to promoters of M1 macrophage genes (Ccl4, Ccl5, Tnf, Il12b).

Conclusions:

  • IRF5 plays a significant role in NEC pathogenesis.
  • IRF5 promotes NEC by driving M1 macrophage polarization.
  • Targeting IRF5 in myeloid cells represents a promising strategy to prevent and treat NEC.

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