Immunologic Arterial Injury and Atherogenesis

  • C. Richard Minick
Conference paper

Abstract

Arterial injury has been shown to be a primary causative factor in arteriosclerosis (Minick et al. 1976; Ross and Glomset 1976). Arterial injury, and the resulting necrosis, inflammation, intimal thickening and other reparative features may favor the deposition of blood-borne lipid at sites of injury and lead to atherosclerosis. It is important to our understanding of the etiology and pathogenesis of human atheorsclerosis to identify those causes of arterial injury and the nature of the reactive change that may be important in etiology and pathogenesis of atherosclerosis in man and other animals. There is considerable evidence to suggest that inflammation of the arterial wall and in particular that resulting from immunologic injury may be important in the development of arteriosclerosis in man. The following observations support this suggestion:
  1. 1.

    Inflammation and atherogenesis share major pathogenic features. Inflammation is a reaction to injury in which there is increased permeability of endothelium of the microcirculation, accumulation of protein-rich fluid in the intersitium, migration of leukocytes, and repair characterized by proliferation of mesenchymal cells and increased connective tissue synthesis. Similarly, necrosis of arterial smooth muscle cells, increased permeability of endothelium, migration of leukocytes, proliferation of mesenchymal cells and increased connective tissue synthesis are all features of atherosclerosis (Joris and Majno 1978).

     
  2. 2.

    Immunological vascular injury and atherosclerosis also share pathogenic features. Increased endothelial permeability resulting from IgE mediated release of vasoactive amines from basophils and platelets is believed to be essential for localization of immune complexes in the arterial wall. Such IgE mediated increases in endothelial permeability may enhance transport of other macromolecules, e.g., lipoproteins, into the arterial wall (Henson and Cochrane 1971). Alterations in endothelium are also important in other types of immunological injury such as graft rejection (Alonso et al. 1977).

     
  3. 3.

    Premature atherosclerosis or atherosclerosis of increased severity has been found in human in association with arterial diseases that have a major inflammatory or immunological components. Saphir et al. (1950) noted evidence of healed arteritis in hearts of humans with premature atherosclerosis and ischemic heart disease. Syphilis, rheumatic heart disease, lupus erythematosus and organ transplantation may be associated with vascular injury, arteritis and premature or unusually severe atherosclerosis (Zeek et al. 1932; Bulkley and Roberts 1975; Rider et al. 1975). There is evidence to indicate that arterial injury in syphilis, rheumatic heart disease, lupus erythematosus and organ transplantation are immunologically mediated.

     

Keywords

Cholesterol Permeability Migration Hepatitis Corticosteroid 

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© Springer-Verlag New York Inc. 1980

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  • C. Richard Minick

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