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Updated: May 28, 2026

Following in Real Time the Impact of Pneumococcal Virulence Factors in an Acute Mouse Pneumonia Model Using Bioluminescent Bacteria
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Pneumococcus uses COMMD2 to alter host cellular immunity.

Michael G Connor1, Lisa Sanchez2, Christine Chevalier3

  • 1Chromatin and Infection Laboratory, Institut Pasteur, Université Paris Cité, Paris, France. mconnor@pasteur.fr.

Nature Communications
|May 26, 2026
PubMed
Summary
This summary is machine-generated.

Streptococcus pneumoniae uses COMMD2 to degrade the NF-κB (nuclear factor kappa B) protein p65, repressing host immunity during infection. This mechanism explains how pathogenic pneumococcus evades the immune response.

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Published on: September 28, 2022

Area of Science:

  • Microbiology
  • Immunology
  • Cellular Biology

Background:

  • NF-κB (nuclear factor kappa B) signaling is crucial for cellular immunity against microbes.
  • Bacteria frequently target the NF-κB pathway during pathogenesis.
  • The role of NF-κB in epithelial responses to Streptococcus pneumoniae, from commensal to pathogenic, remains unclear.

Purpose of the Study:

  • To investigate how Streptococcus pneumoniae modulates NF-κB signaling in epithelial cells.
  • To compare the NF-κB interactome of a commensal-like strain (6B ST90) versus an invasive strain (TIGR4).
  • To elucidate the mechanism by which an invasive pneumococcal strain represses host inflammatory responses.

Main Methods:

  • Comparative mass spectrometry of the p65 interactome.
  • Analysis of host-pathogen interactions between Streptococcus pneumoniae strains and epithelial cells.

Main Results:

  • Invasive TIGR4 strain challenge induced the interaction of COMMD2 with p65 and p62.
  • This complex mediates the export and subsequent degradation of p65.
  • COMMD2 is essential for modulating host cellular immunity during pneumococcal infection.

Conclusions:

  • A novel bacterial pathogenesis mechanism involving COMMD2-mediated degradation of p65 was identified.
  • This mechanism serves to repress the host inflammatory response during Streptococcus pneumoniae infection.
  • The study presents a paradigm for divergent NF-κB responses to pneumococcal strains.