Acute experimental autoimmune encephalomyelitis in mice

Linthicum, D. Scott; Muñoz, J.; Blaskett, Alan C.

doi:10.1016/0008-8749(82)90457-9

Cited by 183 publications

(46 citation statements)

References 23 publications

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“…In previous studies it had been speculated that B. pertussis might increase cerebral vascular permeability (Amiel, 1976). Additionally, the frequently employed enhancement of the induction of experimental autoimmune encephalomyelitis (EAE) by PT has been suggested to be due to an increase in vascular permeability (Ben-Nun et al, 1997) apparently as a consequence of histamine-sensitization (Yong et al, 1993;Linthicum et al, 1982). Recently, it has been reported that whole-cell but not acellular pertussis vaccine induced convulsive activity in mice.…”

Section: Discussionmentioning

confidence: 99%

“…Experimental autoimmune encephalomyelitis (EAE), an accepted model for multiple sclerosis, can be induced in genetically susceptible laboratory animals by a single injection of a central nervous system tissue homogenate or purified myelin antigens. The mechanism by which PT might enhance the development of EAE has not been elucidated but it appears to involve an increase of the vascular permeability of the blood-brain-barrier (Linthicum et al, 1982;Yong et al, 1993;Ben-Nun et al, 1997).…”

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confidence: 99%

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Permeabilization in a cerebral endothelial barrier model by pertussis toxin involves the PKC effector pathway and is abolished by elevated levels of cAMP

Brückener

Bayâ

Galla

et al. 2003

Journal of Cell Science

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Respiratory tract infections caused by Bordetella pertussis are occasionally accompanied by severe neurologic disorders and encephalopathies. For these sequelae to occur the integrity of cerebral barriers needs to be compromised. The influence of pertussis toxin, a decisive virulence factor in the pathogenesis of pertussis disease, on barrier integrity was investigated in model systems for blood-liquor (epithelial) and blood-brain (endothelial)barriers. While pertussis toxin did not influence the barrier function in Plexus chorioideus model systems, the integrity of cerebral endothelial monolayers was severely compromised. Cellular intoxication by pertussis toxin proceeds via ADP-ribosylation of α-Giproteins, which not only interferes with the homeostatic inhibitory regulation of adenylate cyclase stimulation but also results in a modulation of the membrane receptor coupling. Increasing intra-endothelial cAMP levels by employing cholera toxin or forskolin even inhibited the pertussis toxin-induced permeabilization of endothelial barriers. Therefore,pertussis-toxin-induced permeabilization has to be mediated via a cAMP-independent pathway. To investigate potential signalling pathways we employed several well established cellular drugs activating or inhibiting central effectors of signal transduction pathways, such as phosphatidylinositol 3-kinase, adenylate cyclase, phospholipase C, myosin light chain kinase and protein kinase C. Only inhibitors and activators of protein kinase C and phosphatidylinositol 3-kinase affected the pertussis toxin-induced permeability. In summary, we conclude that permeabilization of cerebral endothelial monolayers by pertussis toxin does not depend on elevated cAMP levels and proceeds via the phosphokinase C pathway.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Permeabilization in a cerebral endothelial barrier model by pertussis toxin involves the PKC effector pathway and is abolished by elevated levels of cAMP

Brückener

Bayâ

Galla

et al. 2003

Journal of Cell Science

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“…However, this can only be achieved in certain strains of mice that are notable for increased vascular sensitivity within the central nervous system (87,88). Even in this context disease often requires the use of pertussis toxin that is known to further disrupt the blood-brain barrier (89)(90)(91).…”

Section: Antigens Expressed In Privileged Sitesmentioning

confidence: 99%

The anatomy of T-cell activation and tolerance.

Mondino

Khoruts²,

Jenkins³

1996

Proc. Natl. Acad. Sci. U.S.A.

206

106

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The mammalian immune system must specifically recognize and eliminate foreign invaders but refrain from damaging the host. This task is accomplished in part by the production of a large number of T lymphocytes, each bearing a different antigen receptor to match the enormous variety of antigens present in the microbial world. However, because antigen receptor diversity is generated by a random mechanism, the immune system must tolerate the function of T lymphocytes that by chance express a self-reactive antigen receptor. Therefore, during early development, T cells that are specific for antigens expressed in the thymus are physically deleted. The population of T cells that leaves the thymus and seeds the secondary lymphoid organs contains helpful cells that are specific for antigens from microbes but also potentially dangerous T cells that are specific for innocuous extrathymic self antigens.

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“…EAE can be induced by inoculation with an emulsion of whole spinal cord or brain, or whole or part of a myelin protein, in adjuvant (active EAE). For induction of EAE in mice, Bordetella pertussis toxin is often injected concurrently [9,20,21]. In passively induced EAE, T cells specific for myelin proteins are injected, with or without pertussis toxin.…”

Section: Introductionmentioning

confidence: 99%

A neuropathological analysis of experimental autoimmune encephalomyelitis with predominant brain stem and cerebellar involvement and differences between active and passive induction

Muller

Pender

Greer

2000

Acta Neuropathologica

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Experimental autoimmune encephalomyelitis (EAE) is an autoimmune demyelinating disease that can be induced in a variety of animal species and which is commonly used as an animal model of multiple sclerosis. In rodent EAE models, the clinical disease is typified by ascending paralysis; however, other clinical patterns can also be observed by inducing disease with particular peptides of myelin proteolipid protein (PLP) or myelin oligodendrocyte glycoprotein. Here we describe EAE induced in C3H/HeJ mice by inoculation with residues 190-209 of PLP. This form of EAE is manifested clinically by a movement disorder, with axial rotation of the head and trunk. Histologically, this form of EAE is characterized by predominant cerebellar or brain stem involvement, depending on whether EAE is induced by active immunization with the PLP peptide, or by passive transfer of T cells specific for the peptide. The inflammatory cell infiltrate is composed of polymorphonuclear cells and mononuclear cells. This rotatory form of EAE may be a useful model for studying the neuropathological characteristics of multiple sclerosis affecting the brain stem and cerebellum.

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Acute experimental autoimmune encephalomyelitis in mice

Cited by 183 publications

References 23 publications

Permeabilization in a cerebral endothelial barrier model by pertussis toxin involves the PKC effector pathway and is abolished by elevated levels of cAMP

Permeabilization in a cerebral endothelial barrier model by pertussis toxin involves the PKC effector pathway and is abolished by elevated levels of cAMP

The anatomy of T-cell activation and tolerance.

A neuropathological analysis of experimental autoimmune encephalomyelitis with predominant brain stem and cerebellar involvement and differences between active and passive induction

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