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Epithelial cells maintain memory of prior infection with Streptococcus pneumoniae through di-methylation of histone

Christine Chevalier1, Claudia Chica2, Justine Matheau1,3

  • 1Institut Pasteur, Université Paris Cité, Chromatin and Infection Laboratory, F-75015, Paris, France.

Nature Communications
|July 2, 2024
PubMed

Insights

Bacterial infections leave a lasting epigenetic memory in respiratory epithelial cells. This memory, marked by histone H3 lysine 4 di-methylation (H3K4me2), increases susceptibility to future infections.

Area of Science:

  • Microbiology
  • Epigenetics
  • Respiratory Medicine

Background:

  • Epithelial cells are the primary defense against respiratory pathogens like Streptococcus pneumoniae.
  • The epithelial response to S. pneumoniae and the role of epigenetic modifications are not well understood.
  • Bacterial pathogens can alter host cell transcription through chromatin modifications.

Purpose of the Study:

  • To investigate the epigenetic changes in epithelial cells following Streptococcus pneumoniae infection.
  • To identify specific histone modifications induced by S. pneumoniae infection.
  • To determine if these modifications persist after bacterial clearance and affect subsequent infections.

Main Methods:

  • Analysis of histone modifications in epithelial cells after S. pneumoniae infection.
  • Chromatin immunoprecipitation to detect histone methylation.
  • Assessment of epithelial cell permissiveness to secondary infection.

Main Results:

  • Streptococcus pneumoniae infection induces histone H3 lysine 4 di-methylation (H3K4me2) in epithelial cells.
  • This H3K4me2 modification is maintained for at least 9 days post-antibiotic treatment.
  • The epigenetic program established by infection makes epithelial cells more susceptible to secondary infections.

Conclusions:

  • Bacterial infections establish a persistent epigenetic memory in epithelial cells.
  • H3K4me2 acts as a specific epigenetic mark of infection, distinct from other methylation states.
  • This epigenetic memory alters cellular responses, potentially promoting recurrent infections.

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