Abstract 363: Aortic Walls From Cadavers With Atherosclerosis Show Autoimmune Reactions: Exudation of Proteoglycans, Globulins And Interleukin-17, and Infiltration of Plasma Cells.

Abstract

Athersclerosis is known to be caused by inflammation of aortic intima. In order to elucidate the mechanism of atherosclerosis, we investigated the inflammated changes of media of the ascending aorta associated with coronary artery disease in 44 biopsy specimens. The findings made us confident that inflammation occurs not only in the intima but also in the media of the atherosclerotic aorta, and also made us suspect that atherosclerosis may be caused by an autoimmune reaction. Here, we investigate proteoglycans, globulins, lymphoid cells, and interleukin-17 (IL-17) infiltrating into the wall of atherosclerotic aorta from cadavers, to confirm this idea. Twenty cadavers from 32 to 93 years old were studied. We divided the subjects into 4 groups with 5 cases each: 1-20% as a slight group, 20-50% as a mild group, 50-75% as a moderate group, and 75% or more as a severe group, in terms of the percentage of atheromatous lesion from the ascending to the abdominal aorta. We immunohistochemically stained the ascending aortic wall with antibodies: LY111 for chondroitin-4-sulfate, 2B1 for Versican core protein, LCA and CD4 for lymphocytes, IL17 for cells positive for this, CD68 for macrophage, and CD38 for plasma cells. In addition, using the aortic wall, we delegated the protein electrophoresis demarcation and the measure of the values of IL-17 to a laboratory corporation. Chondroitin-4-sulfate was stained diffusely positive in the entire wall. Versican showed characteristic patchy figure in the media. The numbers of patchy figures were significantly more in the mild and moderate groups than those in the slight and severe groups. In a similar manner, the numbers of plasma cells in the intima and media were significantly more in mild and moderate groups than those in the slight and severe groups. Protein electrophoresis showed the state of chronic inflammation. Among the 4 groups, the values (pg/mg) of IL-17 of mild (307.572±91.341) and moderate (183.027±30.926) groups were significantly increased compared with those of slight (108.310±43.008) and severe (69.812±17.465) groups. The changes of the infiltration of plasma cell, the exudation of proteoglycans and also the increase of IL-17 in the wall make it more confident that atherosclerosis is related to an autoimmune reaction.