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Diffuse Intimal Thickening and Other Mesenchymal Changes

Atherosclerosis is a disease of the arteries that is known to be a focalized growth of the vessel wall into the vessel lumen. A characteristic feature of the atherosclerotic lesion is a massive deposition of lipid within the affected tissue, where inflammatory cells such as monocyte-macrophages are infiltrated forming foam cells. In addition, in the early stage of atherogenesis, proliferation of smooth muscle cells in the intima of the artery is known to be significant. Although intimal smooth muscle cells originate from the media, the cells show high levels of growth activity and production of interstitial collagens compared to those in the media.' Our previous studies on the stromal reaction in inflammatory states such as articular tissue destruction in rheumatoid arthritis and skin diseases have shown that infiltrated polymorphonuclear leukocytes release factor(s) (PMN-factor), the major component of which is now known to be interleukinI p (ILI p)*, stimulate productions of collagenase3 and prostaglandin E, (PGE,)4 of connective tissue cells. These include synovial cells, fibroblasts, chondrocytes,' and even hepatocytes. Both PMN and monocytes from peripheral blood do not contain any stimulating factor of this sort, but can be activated with lipopolysaccharide or zymosan, indicating that inflammatory cells acquire the factor(s) during and/or after infiltration into tissues. In general, members of the IL-I family affect connective tissue cells to stimulate cell proliferation and productions of collagenase and PGE,, but suppress productions of both collagenous and noncollagenous proteins. In this article, we will discuss the effects of inflammatory factors on the cell growth rate and collagen production of smooth muscle cells in culture, and immunolocalization of ILI, interstitial collagenase and tissue inhibitor of rnetalloproteinases (TIMP) in atherosclerotic lesions.