Diverse bacteria promote macrophage foam cell formation via Toll-like receptor-dependent lipid body biosynthesis.

Aim: Atherosclerotic lesions contain DNA signatures from a wide variety of bacteria, although little is known of how exposure to these organisms may modulate the accumulation of lipids in macrophages.

Methods: To address this, a panel of nine bacteria representing those most frequently reported to be present in human atheroma were examined for their potential to promote lipid accumulation in human primary monocytes and murine J774 macrophages.

Results: All bacteria examined, and defined stimulants of Toll-like receptors (TLRs) 2, 3, 4, 5 and 9, induced lipid body formation and cholesterol ester accumulation in a dose-dependent manner.

Toll-like receptor-dependent lipid body formation in macrophage foam cell formation.

Purpose Of Review: The differentiation of macrophages into lipid-laden foam cells is central to the development of atherosclerosis. Traditionally, it has been assumed that the uptake of oxidized low-density lipoprotein by macrophage scavenger receptors is largely responsible for this process. However, in light of recent evidence that these mechanisms may not play as large a role as previously thought, alternative mechanisms of foam cell formation are now being explored.