Commensal Peptoniphilus harei induce activation of monocytes via TLR2/CD14 signalling in whole blood

Tobias Schmidt1,2, Inga-Maria Frick3, Lotta Happonen3

  • 1Division of Pediatrics, Clinical Sciences, Lund University, Lund, Sweden.

PubMed

Insights

Peptoniphilus harei significantly activates monocytes, driving immune responses through CD14 and TLR2 pathways. This highlights the pathogenic potential of these Gram-positive anaerobic cocci in infections.

Area of Science:

  • Immunology
  • Microbiology

Background:

  • Monocytes are key immune cells, but their response to Gram-positive anaerobic cocci (GPAC) is poorly understood.
  • Limited knowledge exists on the inflammatory pathways triggered by GPAC species.

Purpose of the Study:

  • To investigate the capacity of GPAC, specifically Parvimonas micra and Peptoniphilus harei, to activate human monocytes.
  • To elucidate the molecular mechanisms underlying GPAC-induced monocyte activation.

Main Methods:

  • Whole blood stimulation with heat-killed bacteria or conditioned medium (CM).
  • Flow cytometry analysis of monocyte activation markers (PDL1, HLA-DR, CD11b).
  • Assessment of signaling pathway phosphorylation (NFκBp65, p38, Akt) and cytokine production (IL-1β, TNF, IL-6).
  • Mechanistic studies using anti-CD14 and anti-TLR2 antibodies.
  • Mass spectrometry (MS) analysis of CM.

Main Results:

  • Peptoniphilus harei robustly activated monocytes, increasing activation markers, signaling pathway phosphorylation, and cytokine release.
  • Parvimonas micra showed minimal monocyte activation.
  • P. harei-induced activation was partially mediated by CD14 (for whole bacteria) and TLR2 (for CM).
  • MS identified four potential proteins in P. harei CM associated with monocyte activation.
  • Neutrophil activation mirrored monocyte responses.

Conclusions:

  • P. harei induces significant monocyte activation, suggesting pathogenic potential.
  • CD14 and TLR2 are key receptors in P. harei-mediated immune cell activation.
  • These findings expand our understanding of GPAC's role in infectious inflammatory responses.