Journal
JOURNAL OF IMMUNOLOGY
Volume 166, Issue 3, Pages 2018-2024Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.166.3.2018
Keywords
-
Categories
Funding
- NIAID NIH HHS [AI-18797, AI-40275] Funding Source: Medline
Ask authors/readers for more resources
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 I,PS 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-alpha, or IFN-gamma induce TLR2 expression in both human dermal microvessel EC and HUVEC. Furthermore, LPS and IFN-gamma act synergistically to induce TLR2 expression in EC, and LPS-induced TLR2 expression is NF-kappaB dependent. LPS and IFN-gamma 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-alpha, or IFN-gamma. 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-gamma, in inducing shock associated with Gram-negative sepsis.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available