Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infectious agents have often been implicated in the etiology of autoimmune diseases. Here we show that bacteria may also play a role in resistance to autoimmune diseases. SJL/J and (SJL/J x BALB/c)F1 mice are genetically susceptible to induction of experimental autoimmune encephalomyelitis (EAE), a murine model for human demyelinating autoimmune diseases such as multiple sclerosis. We studied the effect of several bacteria on the development of EAE and found that exposure of SJL/J or (SJL/J x BALB/c)F1 mice to Mycobacterium tuberculosis or Bordetella pertussis consistently rendered mice highly refractory to subsequent induction of the disease. Other bacteria such as Escherichia coli, Shigella and Staphylococcus aureus were found to be less effective, or were protective only if specific immunization procedures were used. Furthermore, M. tuberculosis and B. pertussis were protective irrespective of the route of administration and minute amounts (as low as 0.5 micrograms) of M. tuberculosis were sufficient to protect EAE-susceptible mice against induction of the disease. Interestingly, these bacteria, which are commonly used to promote development of EAE, conferred the highest degree of protection against the disease. The M. tuberculosis-induced protection was found to be associated with active suppression mechanisms mediated by T lymphocytes capable of transferring protection to naive syngeneic mice. These findings indicate that certain bacteria may protect against the development of autoimmune diseases. These results also suggest the potential use for still-unidentified bacterial agents in the manipulation of certain autoimmune diseases.
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PMID:Bacterial agents protect against autoimmune disease. I. Mice pre-exposed to Bordetella pertussis or Mycobacterium tuberculosis are highly refractory to induction of experimental autoimmune encephalomyelitis. 148 83

Of 54 Macaca arctoides, 44 died during the 2.5 years after their assignment to a common cage. Although early deaths were due to trauma, acute gastric dilatation, and shigellosis; latter deaths were the result of a variety of uncommon diseases including atypical mycobacterial disease, malignant lymphoma, protozoan encephalomyelitis, and other necrotizing and inflammatory lesions. Atypical mycobacterial disease due to Mycobacterium avium intracellular serotypes was the most frequent single disease agent recognized (33% [18 macaques]). This disease began in the ileum and large intestine with subsequent systemic involvement. An abnormality of host response to infective agents, in general, was indicated by the unusually high occurrence of this disease, as well as other disease processes. Morphologic evaluation of lymphoid organs revealed decreased cellularity of follicles and decreased numbers of plasma cells in all macaques, whereas T cell-dependent areas varied from hypocellular to hypercellular with 5 macaques with malignant lymphoma. The spontaneous erythrocyte rosette-forming subpopulation of T cells was decreased in peripheral blood, but was increased in lymph nodes containing atypical mycobacterial lesions. Serum immunoglobulin value decreased progressively in diseased macaques. A basic abnormality of T-cell subpopulations controlling other components of host response was suspected. Macrophages from lesions that contain mycobacterial organisms did not phagocytize latex beads normally in vitro, whereas monocytes in the blood of the same macaques were capable of in vitro phagocytosis.
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PMID:Immunologic abnormality in a group of Macaca arctoides with high mortality due to atypical mycobacterial and other disease processes. 387 86