Lesion progression and plaque composition are not altered in older apoE-/- mice lacking tumor necrosis factor-alpha receptor p55.

Background: Inflammatory processes are an integral component of the initiation, progression, and destabilization of atherosclerotic lesions. Tumor necrosis factor-alpha (TNF-alpha) is considered a primary mediator of inflammatory processes.

Methods And Results: The role of TNF-alpha in plaque progression and plaque destabilization was investigated in the innominate arteries of older TNF-alpha receptor p55 deficient mice that were generated on a hyperlipidemic apolipoprotein E deficient background (p55-/- apoE-/-). There were no significant differences in levels of circulating cytokines, plaque progression, plaque composition or features of plaque destabilization in p55-/- apoE-/- compared to wild type (p55+/+ apoE-/-) mice.

Conclusions: Progression and destabilization of advanced atherosclerotic lesions does not seem to be mediated via the TNF-alpha receptor p55.