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A Macrophage Reporter Cell Assay to Examine Toll-Like Receptor-Mediated NF-kB/AP-1 Signaling on Adsorbed Protein Layers on Polymeric Surfaces
Published on: January 7, 2020
Increased surface toll-like receptor 2 expression in superantigen shock.
Philip A Hopkins1, Alison C Pridmore, Stephan Ellmerich
1Department of Infectious Diseases, Imperial College, London, UK.
Critical Care Medicine
|April 2, 2008
Summary
Bacterial superantigens up-regulate toll-like receptor 2 (TLR2) on monocytes via MHC class II signaling. This enhanced TLR2 expression may indicate S. pyogenes shock, but TLR2 signaling intensity can decrease in critical illness.
Area of Science:
- Immunology
- Microbiology
- Critical Care Medicine
Background:
- Gram-positive bacterial superantigens are potent immune activators.
- Toll-like receptor 2 (TLR2) plays a crucial role in innate immunity against bacterial pathogens.
- The interaction between superantigens and TLR2 in critical illness is not fully understood.
Purpose of the Study:
- To investigate the interaction between gram-positive bacterial superantigens and TLR2.
- To examine the role of this interaction in health and critical illness.
- To determine the clinical relevance of TLR2 expression in sepsis and shock.
Main Methods:
- Ex vivo laboratory studies using transfected HeLa cells and primary human monocytes.
- Prospective clinical cohort study involving healthy controls and critically ill patients.
- Analysis included cytokine assays, flow cytometry, and quantitative real-time PCR.
Main Results:
- Superantigens did not directly signal through TLR2 ligation.
- Superantigens up-regulated monocyte surface TLR2 expression via MHC class II signaling.
- TLR2 up-regulation was observed in a subset of patients with S. pyogenes sepsis, but TLR2 ligand responses were reduced in all critically ill patients.
Conclusions:
- Monocyte surface TLR2 expression is up-regulated by superantigens through MHC class II signaling.
- Enhanced TLR2 expression may be specific to S. pyogenes-induced shock.
- TLR2 signaling intensity is not always correlated with expression levels, especially in critical illness or at low ligand concentrations.
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