Toll-like receptor 4 mediates endothelial cell activation through NF-κB but is not associated with endothelial dysfunction in patients with rheumatoid arthritis.

Similarly, mRNA levels of IL-6 were reduced; however, they failed to reach statistical significance (p = 0.07) ( figure 2 , middle panel).

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Discussion The main results of our in-vitro investigations are that, in HAEC, TLR4 antagonism with eritoran: 1) inhibits LPS-induced mRNA expression of the inflammatory cytokines IL-6, IL-8, TNFα, and CCL-2, and of the adhesion molecules VCAM and ICAM; 2) inhibits ox-PAPC-induced mRNA expression of IL-8 and of IL-6, albeit to a borderline significant level; and 3) reduces LPS-induced phosphorylation of NF-κB p65 subunit and IκB-α.

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