Infection Acts Synergistically with a High-Fat Diet in the Development of a Proinflammatory and Potentially Proatherogenic Endothelial Cell Environment in an Experimental Model.

Classic atherosclerosis risk factors do not explain all cases of chronic heart disease. There is significant evidence that gut microbiota may influence the development of atherosclerosis. The widespread prevalence of chronic (, ) infections suggests that can be the source of components that stimulate local and systemic inflammatory responses. Elevated production of reactive oxygen species during infection leads to cholesterol oxidation, which drives atherogenesis. The aim of this study is to explore the link between persistent infection and a high-fat diet in the development of proinflammatory conditions that are potentially proatherogenic. An in vivo model of infected with and exposed to an experimental diet was investigated for the occurrence of a proinflammatory and proatherogenic endothelial environment. Vascular endothelial primary cells exposed to components were tested in vitro for oxidative stress, cell activation and apoptosis. The infiltration of inflammatory cells into the vascular endothelium of animals infected with and exposed to a high-fat diet was observed in conjunction with an increased level of inflammatory markers systemically. The arteries of such animals were the least elastic, suggesting the role of in arterial stiffness. Soluble components induced transformation of macrophages to foam cells in vitro and influenced the endothelial life span, which was correlated with Collagen I upregulation. These preliminary results support the hypothesis that antigens act synergistically with a high-fat diet in the development of proatherogenic conditions.