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Staphylococcus aureus activates dendrite elongation in dendritic cells.

Kai Kobata1, Kazuyuki Furuta1, Yuki Ikeya1

  • 1Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University, Japan.

Biochemical and Biophysical Research Communications
|May 29, 2026
PubMed
Summary

Staphylococcus aureus induces dendritic cell (DC) dendrite extension via TLR2, distinct from SCFAs. This pathway cooperates with SCFAs to enhance immune responses and T cell activation.

Keywords:
Antigen presentationButyrateDendrite elongationDendritic cellsERK/PI3K/Cdc42 pathwayHost–microbe interactionsIL-10IL-17Peptidoglycan: TLR2/MyD88 signalingShort-chain fatty acids (SCFAs)Staphylococcus aureusT-cell activation

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Area of Science:

  • Immunology
  • Cell Biology
  • Microbiology

Background:

  • Dendritic cells (DCs) extend dendrites for antigen uptake and presentation.
  • Short-chain fatty acids (SCFAs) were previously shown to promote DC dendrite extension.
  • The role of Staphylococcus aureus in DC morphology and immune signaling requires further investigation.

Purpose of the Study:

  • To investigate the mechanisms by which Staphylococcus aureus induces dendrite extension in DCs.
  • To explore the signaling pathways involved in S. aureus-mediated DC dendrite extension.
  • To understand how S. aureus and SCFAs cooperate to modulate DC function and immune responses.

Main Methods:

  • Utilized DC2.4 cells, live and heat-killed S. aureus, and purified peptidoglycan (PGN).
  • Employed knockout cells lacking TLR2 or MyD88.
  • Investigated the role of ERK, PI3K, and Cdc42 signaling pathways using inhibitors.
  • Assessed antigen uptake and T cell cytokine production (IL-17, IL-10) upon co-stimulation.

Main Results:

  • S. aureus, heat-killed bacteria, and PGN induced dendrite extension in DC2.4 cells.
  • TLR2 and MyD88 were essential for S. aureus-induced dendrite extension, unlike SCFA-induced extension.
  • ERK, PI3K, and Cdc42 signaling pathways are critical for S. aureus-mediated dendrite extension.
  • Co-stimulation with S. aureus and butyrate enhanced dendrite extension, antigen uptake, and T cell IL-17 and IL-10 production.

Conclusions:

  • S. aureus activates ERK/PI3K/Cdc42 signaling via TLR2 recognition of PGN to induce DC dendrite extension.
  • S. aureus utilizes a distinct pathway for DC dendrite extension compared to SCFAs.
  • S. aureus and SCFAs act cooperatively to enhance DC function and downstream immune responses.