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Capsular Serotyping of Streptococcus pneumoniae by Latex Agglutination
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DNA-release by Streptococcus pneumoniae autolysin LytA induced Krueppel-like factor 4 expression in macrophages

Toni Herta1, Aritra Bhattacharyya1, Christian Bollensdorf1

  • 1Department of Internal Medicine/Infectious Diseases and Pulmonary Medicine, Charité - Universitätsmedizin Berlin, Augustenburger Platz 1, 13353, Berlin, Germany.

Scientific Reports
|April 12, 2018
PubMed

Insights

Streptococcus pneumoniae induces KLF4 in macrophages via bacterial DNA, influencing immune responses. This mechanism involves a novel host DNA sensor, promoting a pro-inflammatory macrophage phenotype.

Area of Science:

  • Immunology
  • Microbiology
  • Molecular Biology

Background:

  • Myeloid cell recruitment to the lungs is crucial for pathogen clearance.
  • The regulation of macrophage immune responses during bacterial infection is complex.
  • The role of KLF4 in macrophage response to Streptococcus pneumoniae is not fully understood.

Purpose of the Study:

  • To investigate the mechanism of KLF4 induction in macrophages by Streptococcus pneumoniae.
  • To identify the role of bacterial DNA and host cell sensors in this process.
  • To elucidate the impact of KLF4 on macrophage immune phenotype.

Main Methods:

  • Utilized Streptococcus pneumoniae infection models in macrophages.
  • Employed knockout macrophage models for Toll-like receptor 9 (TLR9), TRIF, MyD88, ASC, STING, and IFNAR.
  • Performed KLF4 knockdown experiments in bone marrow-derived macrophages (BMMs).
  • Analyzed cytokine secretion profiles.

Main Results:

  • Viable pneumococci releasing LytA-dependent DNA induced KLF4.
  • Exogenous bacterial or host DNA partially restored KLF4 induction in deficient pneumococci.
  • TLR9, TRIF, and MyD88 were partially involved; ASC, STING, and IFNAR were not essential.
  • KLF4 knockdown decreased pro-inflammatory cytokine secretion and increased IL-10 release.

Conclusions:

  • Pneumococci-induced KLF4 in macrophages is mediated by a PAMP-DAMP mechanism involving bacterial DNA.
  • A novel host cell DNA sensor appears to be involved in KLF4 induction.
  • KLF4 regulates macrophage phenotype, promoting pro-inflammatory responses and modulating IL-10 production.

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