Bacterial infection remodels the DNA methylation landscape of human dendritic cells

Genome Res. 2015 Dec;25(12):1801-11. doi: 10.1101/gr.192005.115. Epub 2015 Sep 21.

Abstract

DNA methylation is an epigenetic mark thought to be robust to environmental perturbations on a short time scale. Here, we challenge that view by demonstrating that the infection of human dendritic cells (DCs) with a live pathogenic bacteria is associated with rapid and active demethylation at thousands of loci, independent of cell division. We performed an integrated analysis of data on genome-wide DNA methylation, histone mark patterns, chromatin accessibility, and gene expression, before and after infection. We found that infection-induced demethylation rarely occurs at promoter regions and instead localizes to distal enhancer elements, including those that regulate the activation of key immune transcription factors. Active demethylation is associated with extensive epigenetic remodeling, including the gain of histone activation marks and increased chromatin accessibility, and is strongly predictive of changes in the expression levels of nearby genes. Collectively, our observations show that active, rapid changes in DNA methylation in enhancers play a previously unappreciated role in regulating the transcriptional response to infection, even in nonproliferating cells.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • 5-Methylcytosine / analogs & derivatives
  • Bacterial Infections / genetics*
  • Bacterial Infections / immunology
  • Bacterial Infections / metabolism
  • CpG Islands
  • Cytosine / analogs & derivatives
  • Cytosine / metabolism
  • DNA Methylation*
  • Dendritic Cells / immunology
  • Dendritic Cells / metabolism*
  • Dendritic Cells / microbiology*
  • Epigenesis, Genetic
  • Epigenomics / methods
  • Gene Expression Regulation
  • Host-Pathogen Interactions / genetics*
  • Host-Pathogen Interactions / immunology
  • Humans
  • Mycobacterium tuberculosis / immunology
  • Transcription Factors / metabolism
  • Tuberculosis / genetics
  • Tuberculosis / immunology
  • Tuberculosis / metabolism
  • Tuberculosis / microbiology

Substances

  • Transcription Factors
  • 5-hydroxymethylcytosine
  • 5-Methylcytosine
  • Cytosine

Associated data

  • GEO/GSE64173
  • GEO/GSE64175
  • GEO/GSE64177
  • GEO/GSE64179
  • GEO/GSE64181
  • GEO/GSE64182