E4BP4 in macrophages induces an anti-inflammatory phenotype that ameliorates the severity of colitis

Commun Biol. 2024 May 7;7(1):527. doi: 10.1038/s42003-024-06099-4.

Abstract

Macrophages are versatile cells of the innate immune system that work by altering their pro- or anti-inflammatory features. Their dysregulation leads to inflammatory disorders such as inflammatory bowel disease. We show that macrophage-specific upregulation of the clock output gene and transcription factor E4BP4 reduces the severity of colitis in mice. RNA-sequencing and single-cell analyses of macrophages revealed that increased expression of E4BP4 leads to an overall increase in expression of anti-inflammatory genes including Il4ra with a concomitant reduction in pro-inflammatory gene expression. In contrast, knockout of E4BP4 in macrophages leads to increased proinflammatory gene expression and decreased expression of anti-inflammatory genes. ChIP-seq and ATAC-seq analyses further identified Il4ra as a target of E4BP4, which drives anti-inflammatory polarization in macrophages. Together, these results reveal a critical role for E4BP4 in regulating macrophage inflammatory phenotypes and resolving inflammatory bowel diseases.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Basic-Leucine Zipper Transcription Factors / genetics
  • Basic-Leucine Zipper Transcription Factors / metabolism
  • Colitis* / chemically induced
  • Colitis* / genetics
  • Colitis* / immunology
  • Colitis* / metabolism
  • Colitis* / pathology
  • Disease Models, Animal
  • Inflammation / genetics
  • Inflammation / metabolism
  • Macrophages* / immunology
  • Macrophages* / metabolism
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Phenotype
  • Severity of Illness Index

Substances

  • Nfil3 protein, mouse
  • Basic-Leucine Zipper Transcription Factors