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. 1955 Aug 1;102(2):213–236. doi: 10.1084/jem.102.2.213

ALLERGIC NEURITIS: AN EXPERIMENTAL DISEASE OF RABBITS INDUCED BY THE INJECTION OF PERIPHERAL NERVOUS TISSUE AND ADJUVANTS

Byron H Waksman 1, Raymond D Adams 1
PMCID: PMC2136504  PMID: 13242745

Abstract

In experimental allergic encephalomyelitis (EAE), produced by injecting rabbits with whole rabbit spinal cord together with tubercle bacilli and mineral oil, lesions comparable to those seen in the central nervous system are found in the nerve roots, spinal ganglia, and peripheral nerves. When special fractions of bovine white matter are used as antigen in rabbits, the same distribution of lesions is seen but peripheral nerve involvement is relatively less frequent. When rabbit sciatic nerve or spinal ganglia are used as antigen in rabbits, lesions occur only in the roots, ganglia, and peripheral nerves. Lesions are not produced in the central nervous system, nor is there a meningitis. This disease picture has been called experimental allergic neuritis (EAN). The antigenicity of rabbit nerve is not impaired by autoclaving. Sciatic nerve of other mammalian species produces the same disease in rabbits as does rabbit nerve. Optic nerve, used as antigen, produces the typical picture of EAE, not EAN. The optic nerves are not affected in EAN, whereas they commonly contain lesions in EAE. There are differences of symptomatology, referable to the difference in distribution of lesions, between EAE and EAN. The spinal fluid of EAE shows an increase both in the number of cells and in the total protein content. In EAN, the same changes in protein are observed, but usually the cell count remains normal. The cell count appears to be related to the involvement of cerebral and spinal meninges, which is an almost invariable accompaniment of EAE. The skin tests and serologic studies made with homologous and heterologous antigens were essentially non-contributory, apparently as a consequence of the diversity of antigens present in the inoculated materials. The similarity between EAN and certain of the human polyneuritides is indicated and discussed.

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Selected References

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  1. ALVORD E. C., Jr Studies on the etiology and pathogenesis of experimental meningoencephalomyelitis in the guinea pig. J Immunol. 1949 Apr;61(4):355–367. [PubMed] [Google Scholar]
  2. CAMPBELL B., GOOD R. A. Cytopathology of the brain and reticuloendothelial organs in allergic encephalitis in guinea pigs. Arch Neurol Psychiatry. 1950 Feb;63(2):298–310. doi: 10.1001/archneurpsyc.1950.02310200106009. [DOI] [PubMed] [Google Scholar]
  3. GELL P. G. H., HINDE I. T. The histology of the tuberculin reaction and its modification by cortisone. Br J Exp Pathol. 1951 Dec;32(6):516–529. [PMC free article] [PubMed] [Google Scholar]
  4. GOLDSTEIN N. P., KOLB L. C., MASON H. L., SAYRE G. P., KARLSON A. G. Relationship of homologous brain proteolipid to allergic encephalomyelitis in guinea pigs. Neurology. 1953 Aug;3(8):609–614. doi: 10.1212/wnl.3.8.609. [DOI] [PubMed] [Google Scholar]
  5. HAYMAKER W. E., KERNOHAN J. W. The Landry-Guillain-Barré syndrome; a clinicopathologic report of 50 fatal cases and a critique of the literature. Medicine (Baltimore) 1949 Feb;28(1):59–141. [PubMed] [Google Scholar]
  6. HILL K. R. An investigation into the presence of antibodies and hypersensitivity in the encephalitis produced experimentally by the injection of homologous brain suspensions. Bull Johns Hopkins Hosp. 1949 Apr;84(4):302–333. [PubMed] [Google Scholar]
  7. HURST E. W. Experimental demyelination in relation to human and animal disease. Am J Med. 1952 May;12(5):547–560. doi: 10.1016/0002-9343(52)90235-0. [DOI] [PubMed] [Google Scholar]
  8. HURST E. W. Experimental demyelination in relation to human and animal disease. Am J Med. 1952 May;12(5):547–560. doi: 10.1016/0002-9343(52)90235-0. [DOI] [PubMed] [Google Scholar]
  9. INNES J. R. M. Experimental "allergic" encephalitis: attempts to produce the disease in sheep and goats. J Comp Pathol. 1951 Oct;61(4):241–250. doi: 10.1016/s0368-1742(51)80024-9. [DOI] [PubMed] [Google Scholar]
  10. KABAT E. A., WOLF A., BEZER A. E., MURRAY J. P. Studies on acute disseminated encephalomyelitis produced experimentally in rhesus monkeys. J Exp Med. 1951 Jun;93(6):615–633. doi: 10.1084/jem.93.6.615. [DOI] [PMC free article] [PubMed] [Google Scholar]
  11. KABAT E. A., WOLF A., BEZER A. E. Studies on acute disseminated encephalomyelitis produced experimentally in rhesus monkeys. J Exp Med. 1948 Oct 1;88(4):417–426. doi: 10.1084/jem.88.4.417. [DOI] [PMC free article] [PubMed] [Google Scholar]
  12. Kabat E. A., Wolf A., Bezer A. E. THE RAPID PRODUCTION OF ACUTE DISSEMINATED ENCEPHALOMYELITIS IN RHESUS MONKEYS BY INJECTION OF HETEROLOGOUS AND HOMOLOGOUS BRAIN TISSUE WITH ADJUVANTS. J Exp Med. 1947 Jan 1;85(1):117–130. doi: 10.1084/jem.85.1.117. [DOI] [PMC free article] [PubMed] [Google Scholar]
  13. LUMSDEN C. E. Experimental allergic encephalomyelitis. Brain. 1949 Jun;72(Pt 2):198–226. [PubMed] [Google Scholar]
  14. LUMSDEN C. E., KABAT E. A., WOLF A., BEZER A. E. Studies on acute disseminated encephalomyelitis produced experimentally in Rhesus monkeys; complement-fixing antibodies. J Exp Med. 1950 Sep;92(3):253–270. doi: 10.1084/jem.92.3.253. [DOI] [PMC free article] [PubMed] [Google Scholar]
  15. Morgan I. M. ALLERGIC ENCEPHALOMYELITIS IN MONKEYS IN RESPONSE TO INJECTION OF NORMAL MONKEY NERVOUS TISSUE. J Exp Med. 1947 Jan 1;85(1):131–140. doi: 10.1084/jem.85.1.131. [DOI] [PMC free article] [PubMed] [Google Scholar]
  16. Sabin A. B., Aring C. D. Visceral lesions in infectious polyneuritis: (Infectious neuronitis, acute polyneuritis with facial diplegia, guillain-barré syndrome, landry's paralysis). Am J Pathol. 1941 Jul;17(4):469–482.15. [PMC free article] [PubMed] [Google Scholar]
  17. TAL C., OLITSKY P. K. The chemical nature of encephalitogenic proteolipide A and B. Proc Soc Exp Biol Med. 1952 Dec;81(3):590–593. doi: 10.3181/00379727-81-19951. [DOI] [PubMed] [Google Scholar]
  18. THOMAS L., PATERSON P. Y., SMITHWICK B. Acute disseminated encephalomyelitis following immunization with homologous brain extracts; studies on the role of a circulating antibody in the production of the condition in dogs. J Exp Med. 1950 Aug;92(2):133–152. doi: 10.1084/jem.92.2.133. [DOI] [PMC free article] [PubMed] [Google Scholar]
  19. WAKSMAN B. H., MORRISON L. R. Tuberculin type sensitivity to spinal cord antigen in rabbits with isoallergic encephalomyelitis. J Immunol. 1951 Apr;66(4):421–444. [PubMed] [Google Scholar]
  20. WAKSMAN B. H., PORTER H., LEES M. D., ADAMS R. D., FOLCH J. A study of the chemical nature of components of bovine white matter effective in producing allergic encephalomyelitis in the rabbit. J Exp Med. 1954 Nov 1;100(5):451–471. doi: 10.1084/jem.100.5.451. [DOI] [PMC free article] [PubMed] [Google Scholar]
  21. Weil A. J. THE WASSERMANN ANTIGEN AND RELATED "ALCOHOL-SOLUBLE" ANTIGENS. Bacteriol Rev. 1941 Dec;5(4):293–330. doi: 10.1128/br.5.4.293-330.1941. [DOI] [PMC free article] [PubMed] [Google Scholar]

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