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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A time-course study was made of the systemic humoral immune response of Lewis rats to myelin basic protein (BP) as influenced by the dosage of ancillary pertussis adjuvant. Peak activities were observed 5 to 7 weeks after injection. When injected proximal to BP and Mycobacterium butyricum in complete Freund's adjuvant (CFA), Bordetella pertussis at the level of 4 billion organisms doubled the antibody-binding activity of rat sera for 125I-labeled BP as compared to activities obtained with 0, 2, 6, or 8 billion. The severity of clinical symptoms of experimental allergic encephalomyelitis (EAE) at the end of the 2nd week was greatest in rats receiving 64 billion organisms, the very same rats that displayed a severely dampened humoral immune response to BP 5 weeks later. When pertussis was injected i.p. rather than proximal to the CFA mixture, the time-course of the humoral immune response displayed a different profile--unusually high binding activities at the time of onset of EAE that fluctuated back and forth from high to low and that eventually dampened to an intermediate level.
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PMID:The antibody responses to myelin basic protein (BP) in Lewis rats: the effects of Bordetella pertussis. 5 76

Development of hyperacute experimental allergic encephalomyelitis in Lewis rats after intraperitoneal administration of a mixture of guinea pig spinal cord emulsion and pertussigen from Bordetella pertussis was accompanied by an increase in vascular permeability in the central nervous system. The increased permeability was most striking in the spinal cord and seemed to be associated with the ascending development of paralysis. Rats that had completely recovered from paralysis did not have any increased permeability in the central nervous system. Rats which developed paralysis after inoculation with either guinea pig spinal cord emulsion alone or with complete Freund adjuvant had only a small degree, if any, of increased permeability in the vascular system of the central nervous system.
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PMID:Vascular permeability changes in the central nervous system of rats with hyperacute experimental allergic encephalomyelitis induced with the aid of a substance from Bordetella pertussis. 21 Oct 87

Dynamics of emergence of specific reactive cell (SRC) with respect to the brain antigen in the draining regional lymph nodes and peripheral blood was studied in experimental whooping cough allergic encephalomyelitis (EAE) in guinea pigs. The greatest number of SRC in the regional lymph nodes, that markedly decreased by the 9th day of sensitization, was revealed in the middle of the EAE incubation period (the 6-7th day), whereas the peripheral blood showed the highest SRC number during this period. The SRC number rose in the regional lymph nodes and dropped in the peripheral blood at the height of EAE progress (the 20th day). It is concluded that SRC found may be attributed to T lymphocyte population.
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PMID:[Specifically reactive cells in experimental allergic pertussis encephalomyelitis]. 39 Dec 96

In this work we demonstrate a suppressive activity on the induction of experimental allergic encephalomyelitis (EAE) in Lewis rats, transferable to syngeneic animals, challenged with encephalitogenic mixture (myelin basic protein, complete Freud's adjuvant plus Bordetella pertussis organisms) 24 h later. This activity is probably effected by T cells and not by (an) inhibitory serum factor(s). The induction of this specific protection could be due to the penetration of the myelin basic protein antigen into the thymus where we first found suppressive cells. From the thymus, suppressor cells could then emigrate to spleen (on day 15) and to nondraining lymph nodes (on day 17). In the course of normal EAE in Lewis rats and especially at the time of self cure, this suppression is not demonstrated, but possible.
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PMID:Evidence for suppressor cells in Lewis rats' experimental allergic encephalomyelitis. 92 33

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

Numerous experiments have demonstrated that physical stress can alter immunological parameters. However, little attention has been paid to the interrelationship between stress and autoimmune processes. The present study was designed to determine the influence of electric shock and sound stress on the development of experimental allergic encephalomyelitis (EAE). Ten-week-old male DA rats highly susceptible to EAE were used. Rats were subjected to the stress procedure during 19 days either before or after immunization with intradermal injection of 0.1 ml of an emulsion containing guinea pig spinal cord (20 mg/rat) in an equal volume of complete Freund's adjuvant (CFA). In addition, rats received subcutaneous injection of Bordetella pertussis in the dorsum of the same foot. Electric stress procedure consisted of 80 inescapable, unpredictable tail shocks (5 s, 1 mA) delivered at the same time each day. Sound stress procedure consisted of exposure of rats to a 90 dB fire alarm bell which rings 60 times for 5 s during one hour, at the same time of the day. Rats were observed daily for clinical signs of EAE and survived animals were sacrificed on day 20 after immunization. The brain and spinal cord sections were examined histologically for mononuclear cell infiltrates characteristics for EAE. The results clearly indicate that inescapable tail shocks suppressed the appearance and development of EAE when rats were subjected to stress procedure during 19 days after immunization, but not when rats were stressed during 19 day before the induction of EAE. On the other hand, in rats exposed to sound stress there was only delay in the onset of the disease.
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PMID:Stress-induced suppression of experimental allergic encephalomyelitis in the rat. 177 36

A survey was conducted to characterize domestic and exotic bird populations, estimate seroprevalence to selected disease agents, and describe health management practices on 62 premises containing "backyard" flocks located within one mile of 22 commercial California meat-turkey flocks participating in National Animal Health Monitoring System (NAHMS). Chickens were present on 56 backyard premises and turkeys on seven. Antibodies were identified against Mycoplasma gallisepticum, M. synoviae, M. meleagridis, Salmonella pullorum, Newcastle disease virus, avian encephalomyelitis virus, Bordetella avium, hemorrhagic enteritis virus, infectious bronchitis virus, and infectious bursal disease virus in 367 blood samples from 32 backyard premises. Twenty-two owners of backyard premises said they restricted visitor contact with their birds, and two required visitors to wear rubber boots and use boot disinfectant. Owners of seven premises used biologics and/or pharmaceutics for disease prevention. One family member worked on a commercial turkey ranch, but no other contact between owners, relatives, or employees and commercial poultry was reported.
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PMID:Health survey of backyard poultry and other avian species located within one mile of commercial California meat-turkey flocks. 185 24

Wild turkeys (Meleagridis gallopavo silvestris) trapped as part of a relocation program by the Arkansas Game and Fish Commission were tested for selected infectious diseases and parasites. The 45 birds were trapped at four locations in Pope, Scott, and Montgomery counties (Arkansas, USA). Forty-four blood samples for serology, 27 blood smears and 12 fecal samples were collected. Of the serum samples tested, 20 of 44 (45%) were positive for Pasteurella multocida by enzyme-linked immunosorbent assay (ELISA), 42 of 44 (95%) were positive for Bordetella avium by ELISA, and 15 of 44 (34%) were positive for Newcastle disease virus antibody by the hemagglutination inhibition test. All serum samples were negative for Mycoplasma gallisepticum, Mycoplasma synoviae, avian paramyxovirus 3, avian influenza, hemorrhagic enteritis, Marek's disease, avian encephalomyelitis, laryngotracheitis, Salmonella pullorum and Salmonella gallinarum. Haemoproteus meleagridis was found in eight of 27 (30%) and Leucocytozoon smithi in nine of 27 (33%) blood smears; all smears were negative for Plasmodium hermani. Enteric parasites included Ascaridia dissimilis, Heterakis gallinarum, Eimeria dispersa and Raillietina spp. This study was an attempt to document the health status and disease exposure of wild turkeys in Arkansas to aid in managing and preventing the spread of disease agents to wild turkeys and other species of birds.
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PMID:A survey of infectious diseases in wild turkeys (Meleagridis gallopavo silvestris) from Arkansas. 225 Mar 23

Experimental allergic orchitis (EAO) and experimental allergic encephalomyelitis (EAE) are animal models of organ-specific autoimmune disease. In this study, BALB/cByJ and BALB/cAnNCr mice were susceptible to both autoimmune diseases whereas BALB/cJ subline mice were resistant. Disease resistance in BALB/cJ mice did not appear to be a reflection of either (i) a nonspecific generalized impairment of cellular immunity or (ii) an alteration in the phenotypic expression of Bordetella pertussis-induced histamine sensitization, a phenotype which has been shown to be associated with susceptibility to both diseases. Susceptibility to both EAE and EAO was inherited as a dominant trait in F1 hybrid animals. Segregation analysis in a (BALB/cByJ X BALB/cJ) X BALB/cJ backcross population suggested that disease resistance may be associated with a single genotypic difference in a common regulatory gene affecting susceptibility to both diseases. Linkage analysis of the backcross population failed to demonstrate an association of disease resistance with the mutant raf-1b allele carried by BALB/cJ mice. The results of these studies support previous observations that multiple genotypic differences may in fact exist in mice of the BALB/cJ subline and that such differences play a significant role in the genetic control of susceptibility to EAE and EAO.
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PMID:Differential susceptibility to actively induced experimental allergic encephalomyelitis and experimental allergic orchitis among BALB/c substrains. 244 78

To investigate the sequence of immunopathologic events during lesion formation in acute experimental allergic encephalomyelitis (EAE), SJL/J mice were inoculated with isogeneic spinal cord in complete Freund's adjuvant (CFA) and with Bordetella pertussis on Days 1 and 3 postinoculation (PI). Mice were sampled at different time points PI and T cells, T-cell subsets. Ia+ cells, Ig+ cells, albumin, and Ig deposits were localized in frozen sections by the avidin-biotin complex (ABC) method and direct fluorescence. Furthermore, samples were stained for Ia antigen, myelin basic protein (MBP), and galactocerebroside (GC) localization on endothelial cells by the ABC technique. Clinical and pathologic observations were correlated with the immunopathologic results. It was found that early in the disease process myelin and Ia-antigens were demonstrable on endothelial cells within the central nervous system (CNS). Simultaneously, damage to the blood-brain barrier was apparent, as indicated by albumin deposits, and small numbers of infiltrating T cells, T-cell subsets, and Ia+ cells were found. With time PI, the density of infiltrating total T cells (Thy-1.2+), helper/inducer (Lyt-1+), and suppressor/cytotoxic (Lyt-2+) T cells increased; Lyt-1+ and Lyt-2+ cells were detectable in meningeal as well as parenchymal infiltrates, while later on, Lyt-1+ cells showed some predilection for the CNS parenchyma and Lyt-2+ cells for meninges. Ia+ cells (B cells, macrophages, activated T cells) were present in small numbers only. Ig+ cells (B cells and macrophages) appeared shortly before onset of signs and persisted in moderate numbers. These results reconfirm the importance of early T-cell involvement for the development of EAE; they might also indicate a secondary role for Ig+ cells and are consistent with the concept that presentation of myelin antigens to T cells might occur locally on Ia-bearing endothelial cells within the CNS.
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PMID:Acute experimental allergic encephalomyelitis in the mouse: immunopathology of the developing lesion. 257 95


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