Immunologic Injury and Atherosclerosis

  • C. Richard Minick
  • George E. Murphy
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 43)


Injury to the arterial wall is probably a primary causative factor in arteriosclerosis (Anitschkow, 1933; Duff, 1935; Rössle, 1944; Hass, 1955; Taylor, 1955; Waters, 1955; Constantinides, 1965; Minick et al., 1966; Haust, 1971; Minick and Murphy, 1973). Injury, the resulting inflammation, and subsequent repair may favor the deposition and accumulation of blood-borne lipid at the site of injury. Therefore, it is essential for our understanding of human arteriosclerosis to discover the causes of injury and the nature of the local reactive changes that may be important in man. In this regard Dr. McMillan (this publication) reminded us earlier that the reaction of arterial mesenchyme to syphilitic injury could lead to atherosclerosis. Moreover, rheumatic injury to the aorta, heart valves, and coronary arteries can lead to atherosclerosis of these structures (Zeek, 1932; Murphy, unpublished observations, 1973). Data obtained from clinical observations and from experiments indicate that immunological injury plays an important role in the pathogenesis of rheumatic cardiovascular disease (Murphy, 1960) and also may be important in the pathogenesis of syphilitic cardiovascular disease (Chesney, 1926). Finally, immunological reactions are known to cause release of vasoactive substances that may alter vascular permeability and thereby favor deposition of blood-borne lipid in the arterial wall (Kniker and Cochrane, 1965; Cochrane, 1971). Thus, an immunological response to many antigens including those in infecting microorganisms, vaccines, antibiotics, and other drugs, foods, and tobacco, as well as immunological response to substances in one’s own tissues may be an important causative factor in an even greater amount of arterial disease in man, some of which may evolve as athero-arteriosclerosis.


Coronary Atherosclerosis Rheumatic Heart Disease Intimal Thickening Fatty Change Arterial Lesion 


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  1. Alonso, D.R., Starek, P., and Minick, C.R. (1970). Induction of atherosclerosis in transplanted rabbit hearts by the synergy of graft rejection and cholesterol-rich diet. (Abstract). Circulation 42, Suppl. III -5.Google Scholar
  2. Andrus, S.B., and Portman, O.W. (1966). Comparative studies of spontaneous and experimental atherosclerosis in primates. In “Some recent developments in comparative medicine.” (R-.N. T-W-Fiennes, ed.). Zool. Soc., London 17, 161. Academic Press, London.Google Scholar
  3. Anitschkow, N.N. (1933). Experimental arteriosclerosis in animals. In “Arteriosclerosis: A Survey of the Problem” ( E.V. C- owdry, ed.), MacMillan, New York, 271.Google Scholar
  4. Bieber, C.P., Stinson, E.B., Shumway, N.E., Payne, R., and Kosek, J. (1970). Cardiac transplantation in man. VII. Cardiac allograft pathology. Circulation 41, 753.Google Scholar
  5. Chesney, A.M. (1926). Immunity in syphilis. Medicine 5, 537.CrossRefGoogle Scholar
  6. Cochrane, C.G. (1971). Mechanisms involved in the deposition of immune complexes in tissues. J. Exp. Med. 134, 75.Google Scholar
  7. Constantinides, P. (1965). “Experimental Atherosclerosis.” Elsevier Publishing, Amsterdam.Google Scholar
  8. Dock, W. (1946). The predilection of atherosclerosis for the coronary arteries. J. Amer. Med. Ass. 131, 875.Google Scholar
  9. Duff, G.L. (1935). Experimental cholesterol arteriosclerosis and its relationship to human arteriosclerosis. Arch. Pathol. 20, 81; 259.Google Scholar
  10. French, J.E. (1966). Atherosclerosis in relation to the structure and function of the arterial intima, with special reference to the endothelium. Int. Rev. Exp. Pathol. 5, 253.Google Scholar
  11. Gore, I., and Goodman, M.L. (1967). Intimai thickening and dietary atherosclerosis. Arch. Pathol. 84, 49.Google Scholar
  12. Hardin, N.J., Minick, C.R., and Murphy, G.E. (1973).Experimental induction of athero-arteriosclerosis by the synergy of allergic injury to arteries and lipid rich diet.Google Scholar
  13. III. The role of earlier acquired fibromuscular intimai thickening in the pathogenesis of later developing atherosclerosis. Amer. J. Pathol. 73, 301.Google Scholar
  14. Hass, G.M. (1955). Observations on vascular structure in relation to human and experimental arteriosclerosis. In “Symposium on Atherosclerosis.” p. 24. National Academy of Sciences - National Research Council, Washington, D.C.Google Scholar
  15. Hass, G.M., Trueheart, R.E., and Hemmens, A. (1961). Experimental atherosclerosis due to calcific medial degeneration and hypercholesterolemia. Amer. J. Pathol. 38, 289.Google Scholar
  16. Haust, M.D. (1971). Arteriosclerosis. In “A Textbook of Pathology.” ( J.G. Brunson, ed.), p. 451. Macmillan, New York.Google Scholar
  17. Kniker, W.T., and Cochrane, C.G. (1965). Pathogenic factors in vascular lesions of experimental serum sickness. J. Exp. Med. 122, 83.Google Scholar
  18. McMillan, G.C. (This publication). Mesenchymal involvement in arteriosclerosis.Google Scholar
  19. Minick, C.R., and Murphy, G.E. (1973). Experimental induction of athero-arteriosclerosis by the synergy of allergic injury to arteries and lipid-rich diet. II. Effect of repeatedly injected foreigh protein in rabbits fed a lipid-rich, cholesterol-poor diet. Amer. J. Pathol. 73, 265.Google Scholar
  20. Minick, C.R., Murphy, G.E., and Campbell, W.G., Jr. (1966). Experimental induction of athero-arteriosclerosis by the synergy of allergic injury to arteries and lipid-rich diet. I. Effect of repeated injections of horse serum in rabbits fed a dietary cholesterol supplement. J. Exp. Med. 124, 635.Google Scholar
  21. Moss, N.S., and Benditt, E.P. (1970). The ultrastructure of spontaneous and experimentally induced arterial lesions. II. The spontaneous plaque in the chicken. Lab. Invest. 23, 231.Google Scholar
  22. Movat, H.Z., More, R.H., and Haust, M.D. (1958). The diffuse intimal thickening of the human aorta with aging. Amer. J. Pathol. 34, 1023.Google Scholar
  23. Murphy, G.E. (Unpublished observations, 1973 ). Observations indicating that rheumatic injury to coronary arteries leads in some cases to precocious or later developing atheroarteriosclerosis in these arteries: A microscopic study of coronary arteries of infants, children, adolescents, and adults with rheumatic heart disease.Google Scholar
  24. Murphy, G.E. (1960). Nature of rheumatic heart disease, with special fererence to myocardial disease and heart failure. Medicine 39, 289.PubMedGoogle Scholar
  25. Murphy, G.E., Minick, C.R., and Alonso, D.R. ( Unpublished observations, 1973 ). Comparative histologic study of the coronary arteries in human cardiac allografts and hearts of rabbits repeatedly injected with foreign protein and fed a lipid-rich diet.Google Scholar
  26. ROssle, R. (1944). Úber die Serosen Entzundungen der Organe. Virchows Arch. Pathol. Anat. 311, 252.Google Scholar
  27. Ssolowjew, A. (1930). Experimentelle Untersuchungen über die Bedeutung von Localer Schâdigung far die Lípoidablagerung in der Arterienwand. Z. Gesamte Exp. Med. 69, 94.Google Scholar
  28. Taylor, C.G. (1955). The reaction of arteries to injury by physical agents, with a discussion of arterial repair and its relationship to atherosclerosis. In “Symposium on Atherosclerosis.” p. 74. National Academy of Sciences - National Research Council, Washington, D.C.Google Scholar
  29. Taylor, C.B., Trueheart, R.E., and Cox, G.E. (1963). Atherosclerosis in rhesus monkeys. III. The role of increased thickness of arterial walls in atherogenesis. Arch. Pathol. 76, 14.Google Scholar
  30. Thompson, J.G. (1969). Production of severe atheroma in a transplanted human heart. Lancet 2, 1088.CrossRefGoogle Scholar
  31. Waters, L.L. (1955). The reaction of the artery wall to injury by chemicals or infection. In “Symposium on Atherosclerosis.” p. 91. National Academy of Sciences - National Research Council, Washington, D.C.Google Scholar
  32. Wilens, S.L. (1951). The nature of diffuse intimai thickening of arteries. Amer. J. Pathol. 27, 825.Google Scholar
  33. Zeek, P. (1932a). Studies in atherosclerosis. I. Conditions in childhood which predispose to the early development of arteriosclerosis. Amer. J. Med. Sci. 184, 350.Google Scholar
  34. Zeek, P. (1932b). Studies in atherosclerosis. II. Atheroma and its sequelae in rheumatic heart disease. Amer. J. Med. Sci. 184, 356.Google Scholar

Copyright information

© Plenum Press, New York 1974

Authors and Affiliations

  • C. Richard Minick
    • 1
  • George E. Murphy
    • 1
  1. 1.Department of PathologyThe New York Hospital-Cornell Medical CenterNew YorkUSA

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