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)

Administration of Bordetella pertussis vaccine simultaneously with the immunization of rats with guinea pig encephalitogenic protein in Freund's complete adjuvant results in the development of hyperacute encephalomyelitis in the Lewis strain, a strain which reacts with ordinary experimental autoimmune encephalomyelitis (EAE) when immunization is performed without pertussis vaccine. A marked augmentation of the EAE response was seen with pertussis vaccine in the Fischer and PVG strains, both low responders without pertussis, and relapsing EAE developed in some animals. Hyperacute EAE did not develop, however. No effect was seen on the resistant BN strain, but strong EAE developed in the otherwise low-susceptible F1(BN X F) and the practically resistant F2(BN X F) hybrids - in the latter hybrids, EAE developed only when Ir-EAE genes linked to AgB 1 were present. In the F1 hybrids, pertussis vaccine could be given from 4 days before to 5 days after the immunization and an effect was still seen, although a maximal effect was seen when the vaccine was given at 0 or 2 days after immunization.
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PMID:Effect of Bordetella pertussis vaccine on experimental autoimmune encephalomyelitis in rats. 348 80

A hyperacute form of experimental allergic encephalomyelitis (EAE) has been produced previously by administering pertussis vaccine to rats actively immunized with neural antigen or given passive transfer of lymphoid cells from donors with EAE. Now, a localized form of hyperacute EAE has been produced within 1 day of passive transfer. The speed with which pertussis acts tends to exclude antibody production as the mechanism for conversion of EAE to the hyperacute form. With this rapid system, it has been found that pertussis, or its histamine-sensitizing factor, inhibited the host mononuclear cell component of the pervascular lesions. When the immune injury was sufficiently severe (high doses of donor EAE cells), the decrease in the number of mononuclear cells was accompanied by an increase in the amount of fibrin and the number of neutrophils in the lesions. This inverse relationship may be explained by the loss of the protective effect of mononuclear cells on vessels, a concept for which there is increasing evidence.
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PMID:Hyperacute allergic encephalomyelitis. A localized form produced by passive transfer and pertussis vaccine. 458 27

The nature and specificity of the mononuclear cells in passively transferred autoimmune encephalomyelitis and adrenalitis were studied. The recipients were prepared by production of a small heat lesion in the target tissue 5 days before transfer. Within 24 hr after transfer of lymph node cells from donors sensitized with the corresponding tissue antigen, a dense mononuclear cell infiltrate developed around the lesion. When lymph node cells labeled in vitro with (3)H-thymidine or (3)H-adenosine were transferred, a significant number of labeled lymphocytes was found in the infiltrate at 24 or 48 hr. Lymphocytes labeled with (3)H-thymidine showed a greater tendency to accumulate than cells labeled with (3)H-adenosine, indicating that newly formed lymphocytes were more prone to enter the reaction than older cells. Labeled lymphocytes and macrophages of recipient origin and labeled lymphocytes from donors stimulated with B. pertussis were also shown to accumulate around the heat lesion provided the reaction had been initiated by transfer of unlabeled lymphocytes from donors sensitized to the appropriate tissue-specific antigen. In recipients which were given lymph node cells from two groups of donors, sensitized either to spinal cord or to adrenal antigens, with cells from only one group of donors labeled, equal percentages of labeled cells were found around each lesion. Thus, no evidence of preferential accumulation of specifically sensitized lymphocytes was obtained. In recipients which received whole body irradiation on the day of production of the heat lesions, 5 days before transfer of lymph node cells from appropriately sensitized donors, neither monocytes nor lymphocytes accumulated around the lesion. However, if the tibial bone marrow was shielded or if bone marrow cells were given to the recipients shortly after irradiation, inflammation developed as in normal recipients. In recipients which were irradiated 24 hr after the transfer of unlabeled lymph node cells from donors sensitized to the appropriate tissue antigen and then given labeled lymph node cells from B. pertussis-stimulated donors, labeled lymphocytes were found in the reaction 24 hr later. This accumulation occurred although virtually all the lymphocytes present in the lesion at 24 hr after the first transfer were destroyed by the irradiation. The results are interpreted as follows. The autoimmune reaction is initiated by the arrival at the site of a few specifically sensitized lymphocytes, probably on a random basis. After contact with antigen, factors are produced and released which cause the influx of monocytes and of lymphocytes, in particular newly formed ones, of various specificities. There is no preferential accumulation of specifically sensitized cells. The influx of lymphocytes appears to require the presence of monocytes or macrophages in the reaction.
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PMID:The nature and the specificity of mononuclear cells in experimental autoimmune inflammations and the mechanisms leading to their accumulation. 557 33

Addressed are the features of postviral and postvaccinial syndromes affecting the CNS. The relationships among acute disseminated encephalomyelitis, EAE, and MS are discussed. Among the postvaccination syndromes covered are the neurologic sequelae of pertussis immunizations, with a description of a mouse model of this encephalopathy.
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PMID:Postinfectious and postvaccinial encephalomyelitis. 615 Apr 30

SJL/J, PL/J, and (SJL/J x PL/J)F1 mice were immunized with bovine, guinea pig, mouse, or rat myelin basic proteins (MBP) in adjuvant containing Mycobacterium tuberculosis H37Ra. Twenty-four and 72 hr later, Bordetella pertussis vaccine was given i.v. All MBP tested induced experimental allergic encephalomyelitis (EAE) in SJL/J and F1 mice; however, bovine MBP was inactive in PL/J mice. Each strain was immunized in a similar manner with peptic peptides, residues 1-37, 43-88, and 89-169 of guinea pig MBP. In contrast to the SJL/J strain, which has been shown to recognize a major encephalitogenic determinant in peptide 89-169, PL/J and F1 mice responded primarily to an encephalitogenic determinant within peptide 1-37. Analysis of antibody levels showed that SJL/J mice made no antibody to peptide 1-37, although anti-peptide 89-169 antibodies were consistently found. Conversely, PL/J mice responded well to peptide 1-37, but only an occasional animal made a significant response to peptide 89-169. (SJL/J x PL/J)F1 mice were more susceptible to EAE than either parental strain, as shown by the percentage of animals showing neurologic signs and by clinical severity.
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PMID:Induction of experimental allergic encephalomyelitis in PL/J and (SJL/J x PL/J)F1 mice by myelin basic protein and its peptides: localization of a second encephalitogenic determinant. 618 47

Murine T-cell lines derived from (SJL/J X BALB/c)F1 mice were established which are specifically proliferating in response to myelin basic protein (BP) and are also functional in mediating experimental autoimmune encephalomyelitis (EAE) in normal recipients. Partial characterization of the cells, the requirements of their selection and in vitro activation, and the role of pertussis vaccine for mediation of EAE were studied. The EAE-effector line cells were characterized as Lyt 1+2- cells, suggesting delayed-type hypersensitivity mechanism as a major EAE-effector mechanism in mice. Activation in vitro of EAE-effector line cells by stimulation with BP or concanavalin A in the presence of irradiated syngeneic accessory cells was required to facilitate their capacity to mediate EAE in normal recipients. (SJL/J X BALB/c)F1 EAE-effector line cells recognize BP presented by F1-specific accessory cells to facilitate adequate specific proliferation of the cells. Pertussis vaccine was found nonessential for mediation of EAE by BP-specific effector line cells, but was found essential for uncovering T cells responding to BP. Thus, the pertussis vaccine may play a more crucial role at the sensitization phase, by enhancing a T-cell response to BP, rather than by altering the blood-brain barrier at the effector phase of EAE.
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PMID:Experimental autoimmune encephalomyelitis mediated by T-cell line. II. Specific requirements and the role of pertussis vaccine for the in vitro activation of the cells and induction of disease. 619 19

Experimental allergic encephalomyelitis (EAE) is an autoimmune syndrome that can be induced in Lewis rats by myelin basic protein (BP) in complete Freund's adjuvant (CFA). Rats that have recovered from a primary episode of EAE display paradoxical long-term resistance to EAE reinduction by BP-CFA. Previous observations indicated, however, that clinical disease could be reinduced in convalescent rats by a concomitant secondary challenge with BP-CFA + Bordetella pertussis extract (PERT). Vascular permeability changes in the central nervous system (CNS) paralleled disease reinduction. To further probe the relationship between disease reinduction and vascular permeability, convalescent rats were treated with the vasoactive amine antagonist cyproheptadine (CYP) prior to a secondary challenge with BP-CFA + PERT. Data presented here indicate that CYP treatment results in substantial protection of convalescent rats from clinical disease reinduction by BP-CFA + PERT. CYP did not, however, prevent the development of new CNS lesions. CYP therapy also altered the clinical course of EAE induced by a primary injection of BP-CFA + PERT. In these rats, there was a delay in the onset of clinical signs as well as in the appearance of CNS lesions. Nevertheless, both CYP-treated and untreated naive rats challenged with BP-CFA + PERT eventually developed severe and usually lethal EAE. The effect of CYP on EAE induced in naive rats without including PERT in the sensitization protocol was also evaluated. In contrast to the mitigating effect of CYP on EAE induced or reinduced by BP-CFA + PERT, CYP treatment did not affect the clinical course or the development of CNS lesions in rats challenged with BP-CFA alone. Likewise, the passive transfer of EAE, mediated by mitogen-stimulated cells obtained from BP-CFA-sensitized donors, was not affected by CYP treatment. Collectively, these data indicate that CYP therapy altered the expression of EAE induced by regimens that included PERT, but did not affect EAE induced without PERT. In view of the opposing effects of PERT and CYP on vascular permeability, these data are consistent with the hypothesis that alterations in vascular permeability may play a crucial role in controlling the expression of autoimmune neurological diseases.
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PMID:Modification of the clinical and histopathologic expression of experimental allergic encephalomyelitis by the vasoactive amine antagonist cyproheptadine. 620 Dec 89

We studied various biological activities of crystalline pertussigen and found that in mice as little as 0.5 ng of pertussigen induced hypersensitivity to histamine, 8 to 40 ng induced leukocytosis, 2 ng increased production of insulin, 0.1 ng increased production of immunoglobulin E and immunoglobulin G1 antibodies to hen egg albumin, 9.5 ng increased susceptibility to anaphylactic shock, and 0.5 ng increased the vascular permeability of striated muscle. We also found that in Lewis rats 20 ng of pertussigen promoted the induction of hyperacute experimental allergic encephalomyelitis. Pertussigen given intraperitoneally was toxic to mice at a dose of 546 ng. Treatment of pertussigen with glutaraldehyde eliminated this toxicity. Mice immunized with 1,700 ng of detoxified pertussigen were protected against intracerebral challenge with 3 x 10(4) viable Bordetella pertussis cells. When as little as 0.5 ng of pertussigen was given intravenously to mice, the increased susceptibility of the animals to histamine could still be detected 84 days later. The biological properties of crystalline pertussigen indicate its similarity to leukocytosis-promoting factor, Islet-activating protein, late-appearing toxic factor, and mouse-protective antigen of B. pertussis.
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PMID:Biological activities of crystalline pertussigen from Bordetella pertussis. 626 99

The development of acute experimental autoimmune encephalomyelitis (EAE) in mice is potentiated by the use of Bordetella pertussis vaccine as an adjuvant. Histamine sensitizing factor (HSF) extracted from B. pertussis is the active adjuvant agent and causes a mild increase in cerebrovascular permeability. During the development of EAE, there is an additional increase in vascular permeability of the brain and spinal cord. The adjuvant action of B. pertussis HSF does not appear to mimic a generalized beta-adrenergic blockade, since the course of EAE is not potentiated by adrenalectomy. The cerebrovascular permeability changes observed in EAE are probably mediated by vasoactive amines, since the expression of EAE can be blocked by vasoactive amine antagonists.
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PMID:Development of acute autoimmune encephalomyelitis in mice: factors regulating the effector phase of the disease. 629 Mar 79

B. pertussis protein fraction obtained by precipitation with trichloroacetic acid (TCA) stimulated the development of clinically and histologically pronounced experimental allergic encephalomyelitis (EAE) in guinea pigs when introduced together with a heterologous cerebral antigen, the two compounds forming an encephalitogenic mixture. The adjuvant activity of the TCA-precipitated fraction depended on its dose. The sera of the animals with EAE induced by the encephalitogenic mixture containing B. pertussis cells or TCA-precipitated fraction showed a cytopathogenic effect in the monolayer culture of newborn rat cerebellum cells. The cytopathogenic effect was more pronounced in the sera obtained at the period of the development of the clinical symptoms of the disease (days 14-18), while the cytotoxic effect of the sera obtained on day 30 after immunization decreased irrespective of the manifestations of EAE, this decrease being in correlation with the dose of the TCA-precipitated fraction in the encephalitogenic mixture.
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PMID:[Role of the protein fraction of Bordetella pertussis in inducing experimental allergic encephalomyelitis]. 630 Nov 73


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