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Figure 9. Stimulation of mononuclear cells to form foam cells. Infection of mononuclear cells by bacterial pathogens sets in motion a series of events that lead to monocyte activation. Several pathogens epidemiologically linked to the acceleration of atherosclerosis have demonstrated the ability to elicit macrophages to form into foam cells—lipid-laden cells that possess a foamy appearance due to lipid accumulation and are the cells characteristic of an early-stage atheroma called the fatty streak. Recent studies have demonstrated that P. gingivalis stimulates macrophage foam cell formation, and this process appears to be dependent on the attachment of this organism to the macrophage. As part of the characteristic host response of macrophages to infection, these cells express elevated levels of CAMs (green trapezoid) that increase the adhesiveness of these cells to endothelial cells. Additionally, these cells express elevated levels of cytokines and chemokines, as well as TLRs (blue triangles), that could increase macrophage localization to the site of this infected macrophage, as well as increase the sensitivity of these macrophages to specific PAMPs. Ultimately, these mononuclear cells could go on to develop into foam cells as a result of the uptake of serum lipids, including ox-LDL.
