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Tissue-specific transcription factors contribute to diverse cellular functions in mammals. For example, the gene for beta globin, a major component of hemoglobin, is present in all cells of the body. However, it is only expressed in red blood cells because the transcription factors that can bind to the promoter sequences of the beta globin gene are only expressed in these cells. Tissue-specific transcription factors also ensure that mutations in these factors may impair only the function of...
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The eukaryotic promoter region is a segment of DNA located upstream of a gene. It contains an RNA polymerase binding site, a transcription start site, and several cis-regulatory sequences.  The proximal promoter region is located in the vicinity of the gene and has cis-regulatory sequences and the core promoter. The core promoter is the binding site for RNA polymerase and is usually located between -35 and +35 nucleotides from the transcription start site. The distal promoter regions are...
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The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a...
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Updated: Feb 14, 2026

Development and Assessment of Intracellular Infection Models for Staphylococcus aureus
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Development and Assessment of Intracellular Infection Models for Staphylococcus aureus

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Staphylococcus aureus-induced complement activation promotes tissue factor-mediated coagulation.

E W Skjeflo1,2, D Christiansen1, H Fure1

  • 1Research Laboratory, Nordland Hospital, Bodø, Norway.

Journal of Thrombosis and Haemostasis : JTH
|February 14, 2018
PubMed
Summary
This summary is machine-generated.

Staphylococcus aureus infection triggers blood coagulation via complement system activation, specifically C5a-induced tissue factor production. Inhibiting complement component C5 significantly reduced this effect, highlighting complement

Keywords:
Staphylococcus aureusToll-like receptorbacteremiablood coagulationcomplement system proteinstissue factor

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Area of Science:

  • Immunology
  • Hematology
  • Microbiology

Background:

  • Extensive cross-talk exists between the complement system, Toll-like receptors (TLRs), and hemostasis.
  • Consumptive coagulopathy, marked by increased tissue factor (TF) expression, is a hallmark of sepsis.
  • Staphylococcus aureus bacteremia involves complex interactions between these systems.

Purpose of the Study:

  • To investigate the roles of complement, TLRs, and TF in Staphylococcus aureus-induced coagulation.
  • To elucidate the mechanisms of thromboinflammation in a human whole-blood model.

Main Methods:

  • Human whole blood was incubated with S. aureus strains (Cowan, Wood, Newman).
  • Specific inhibitors were used: compstatin (C3), eculizumab (C5), peptide inhibitors (C5aR1, FXII), and neutralizing antibodies (CD14, TLR2, TF), eritoran (TLR4).
  • Measurements included complement activation (ELISA), coagulation markers (PTF1+2 ELISA), and TF expression/activity (qPCR, flow cytometry, ELISA).

Main Results:

  • S. aureus induced significant C5a generation, complement activation, TF production, and coagulation.
  • Inhibition of C5 cleavage was most effective in reducing coagulation markers and TF activity.
  • Complement inhibition's effect was dependent on C5a receptor 1 (C5aR1) and potentiated by CD14 or TLR2 inhibition.

Conclusions:

  • Staphylococcus aureus-induced coagulation in human whole blood is primarily driven by C5a-mediated TF upregulation.
  • The complement system is a key mediator in S. aureus-induced coagulation.
  • Combined inhibition strategies targeting complement and TF show potential for managing thromboinflammation.