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Rapid tissue factor induction by oral streptococci and monocyte-IL-1beta

C-L Hahn1, A M Best, J G Tew

  • 1Department of Endodontics, School of Dentistry, Richmond, VA 23298-0566, USA.

Journal of Dental Research
|February 23, 2007
PubMed

Insights

Oral streptococci rapidly induce interleukin-1beta (IL-1beta), a key cytokine that promotes blood clotting and inflammation. This early inflammatory response may initiate the development of viridans endocarditis.

Area of Science:

  • Immunology
  • Cardiovascular Biology
  • Microbiology

Background:

  • Pro-inflammatory cytokines are known to promote blood coagulation.
  • Viridans group streptococci are a common cause of infective endocarditis.

Purpose of the Study:

  • To investigate the role of pro-inflammatory cytokines induced by oral streptococci in the pathogenesis of viridans endocarditis.
  • To identify specific cytokines involved in early endothelial activation.

Main Methods:

  • Peripheral blood mononuclear cell (PBMC) cultures were stimulated with oral streptococci.
  • Supernatant fluids were analyzed for cytokine activity, particularly endothelial tissue factor (TF) induction.
  • Neutralizing antibodies and recombinant cytokines were used to confirm the role of interleukin-1beta (IL-1beta).
  • Expression of endothelial adhesion molecules (ICAM-1, E-selectin) was assessed.

Main Results:

  • Interleukin-1beta (IL-1beta) was identified as a major early inducer of endothelial tissue factor (TF) activity.
  • Recombinant IL-1beta mimicked the TF-inducing activity of PBMC supernatants.
  • IL-1beta-rich supernatants upregulated endothelial ICAM-1 and E-selectin expression.
  • These adhesion molecules may facilitate the trapping of monocytes and dendritic cells at the infection site.

Conclusions:

  • Oral streptococci rapidly induce IL-1beta production by PBMCs.
  • This rapid IL-1beta induction contributes to early endothelial activation and TF expression.
  • The findings suggest a mechanism by which oral streptococci promote bacterial deposition in fibrin clots, initiating endocarditis.

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