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Induce Toll-Like Receptor 2 and Toll-Like Receptor 4 Expression in Human Endothelial Cells: Role of NF-
B Activation1
*
Division of Pediatric Infectious Diseases, Ahmanson Department of Pediatrics, Steven Spielberg Pediatric Research Center and
Division of Cardiology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA 90048; and
Department of Microbiology and Immunology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814
Toll-like receptor (TLR) 4 has been identified as the primary
receptor for enteric LPS, whereas TLR2 has been implicated as the
receptor for Gram-positive and fungal cell wall components and for
bacterial, mycobacterial, and spirochetal lipoproteins. Vascular
endothelial cell (EC) activation or injury by microbial cell wall
components such as LPS is of critical importance in the development of
sepsis and septic shock. We have previously shown that EC express
predominantly TLR4, and have very little TLR2. These cells respond
vigorously to LPS via TLR4, but are unresponsive to lipoproteins and
other TLR2 ligands. Here we show that LPS, TNF-
, or IFN-
induce
TLR2 expression in both human dermal microvessel EC and HUVEC.
Furthermore, LPS and IFN- act synergistically to induce TLR2
expression in EC, and LPS-induced TLR2 expression is NF-
B dependent.
LPS and IFN- also up-regulate TLR4 mRNA expression in EC. These data
indicate that TLR2 and TLR4 expression in ECs is regulated by
inflammatory molecules such as LPS, TNF-, or IFN-. TLR2 and TLR4
molecules may render EC responsive to TLR2 ligands and may help to
explain the synergy between LPS and lipoproteins, and between LPS and
IFN-, in inducing shock associated with Gram-negative
sepsis.
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