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Lipopolysaccharides from atherosclerosis-associated bacteria antagonize TLR4, induce formation of TLR2/1/CD36 complexes in lipid rafts and trigger TLR2-induced inflammatory responses in human vascular endothelial cells
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posted on 2023-06-08, 08:05 authored by Martha Triantafilou, Frederick G J Gamper, Philipp M Lepper, Marios-Angelos Mouratis, Christian Schumann, Evlambia Harokopakis, Robert E Schifferle, George Hajishengallis, Kathy TriantafilouInfection with bacteria such as Chlamydia pneumonia, Helicobacter pylori, or Porphyromonas gingivalis may be triggering the secretion of inflammatory cytokines that leads to atherogenesis. The mechanisms by which the innate immune recognition of these pathogens could lead to atherosclerosis remain unclear. In this study, using human vascular endothelial cells or HEK293 cells engineered to express pattern-recognition receptors (PRRs), we set out to determine Toll-like receptors (TLRs) and functionally associated PRRs involved in the innate recognition of and response to LPS from H. pylori or P. gingivalis. Using siRNA interference or recombinant expression of cooperating PRRs, we show that H. pylori and P. gingivalis LPS-induced cell activation is mediated through TLR2. Human vascular endothelial cell activation was found to be lipid-raft dependent and to require the formation of heterotypic receptor complexes comprising of TLR2, TLR1, CD36 and CD11b/CD18. In addition, we report that LPS from these bacterial strains are able to antagonise TLR4. This antagonistic activity of H. pylori or P. gingivalis LPS, as well as their TLR2 activation capability may be associated with their ability to contribute to atherosclerosis.
History
Publication status
- Published
Journal
Cellular MicrobiologyISSN
1462-5822External DOI
Issue
8Volume
9Page range
2030-2039Pages
10.0Department affiliated with
- Biochemistry Publications
Notes
Designed work, performed 80% of work, wrote paper.Full text available
- No
Peer reviewed?
- Yes
Legacy Posted Date
2012-02-06Usage metrics
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