Chronic experimental allergic neuritis (EAN) in juvenile guinea pigs: Immunological comparison with acute EAN in adult guinea pigs

Suzumura, Akio; Sobue, Gen; Sugimura, Kimiya; Matsuoka, Yukihiko; Sobue, I

doi:10.1111/j.1600-0404.1985.tb03214.x

Cited by 8 publications

(5 citation statements)

References 26 publications

(16 reference statements)

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“…The chronic relapsing or biphasic experimental autoimmune neuritis, induced in susceptible strains of guinea pigs, rabbits and rats by inoculation with exogenous bovine peripheral nerve myelin or myelin peptides with chronic immune activation facilitated by adjuvants or drugs have been described with variable rates of disease recurrence [128,83,57,86,17]. More recently a murine model of severe chronic demyelinating neuritis with axonal loss akin to progressive CIDP, spontaneous autoimmune peripheral polyneuropathy (SAPP), has been described in non-obese diabetic mice (a mouse strain genetically predisposed to autoimmunity) deficient in CD86, ICAM-1 and autoimmune regulator with cellular and humoral immune responses directed against myelin protein zero associated with altered antigen specific T lymphocyte costimulation or deficient generation of antigen specific regulatory T lymphocytes [124].…”

Section: Introductionmentioning

confidence: 99%

Inflammatory neuropathies: pathology, molecular markers and targets for specific therapeutic intervention

Ubogu

2015

Acta Neuropathol

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Inflammatory neuropathies encompass groups of heterogeneous disorders characterized by pathogenic immune-mediated hematogenous leukocyte infiltration of peripheral nerves, nerve roots or both, with resultant demyelination or axonal degeneration or both. Inflammatory neuropathies may be divided into three major disease categories: Guillain-Barré syndrome (particularly the acute inflammatory demyelinating polyradiculoneuropathy variant), Chronic inflammatory demyelinating polyradiculoneuropathy and nonsystemic vasculitic neuropathy (or peripheral nerve vasculitis). Despite major advances in molecular biology, pathology and genetics, the pathogenesis of these disorders remains elusive. There is insufficient knowledge on the mechanisms of hematogenous leukocyte trafficking into the peripheral nervous system to guide the development of specific molecular therapies for immune-mediated inflammatory neuropathies compared to disorders such as psoriasis, inflammatory bowel disease, rheumatoid arthritis or multiple sclerosis. The recent isolation and characterization of human endoneurial endothelial cells that form the blood-nerve barrier provides an opportunity to elucidate leukocyte-endothelial cell interactions critical to the pathogenesis of inflammatory neuropathies at the interface between the systemic circulation and peripheral nerve endoneurium. This review discusses our current knowledge of the classic pathological features of inflammatory neuropathies, attempts at molecular classification and genetic determinants, the utilization of in vitro and in vivo animal models to determine pathogenic mechanisms at the interface between the systemic circulation and the peripheral nervous system relevant to these disorders and prospects for future potential molecular pathology biomarkers and targets for specific therapeutic intervention.

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Section: Introductionmentioning

confidence: 99%

Inflammatory neuropathies: pathology, molecular markers and targets for specific therapeutic intervention

Ubogu

2015

Acta Neuropathol

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“…The adult guinea pig is an excellent experimental model for studying vestibulocochlear and superior vestibular nerves because it is similar to humans. Experimental models of infection and autoimmune diseases of the nervous system have been studied in adult guinea pigs (Goksu et al, 1992; Qin & Guan, 1997; Sehitoclu et al, 1990; Suzumura et al, 1985; Vasconcelos & Barreira, 2003; Wysocki, 2004). Our findings are consistent with those of other studies (Gacek & Grant, 1961).…”

Section: Discussionmentioning

confidence: 99%

Morphological and morphometric study of the superior vestibular nerve trunk in guinea pigs

Vasconcelos

Schiavoni

Hyppolito

et al. 2022

The Anatomical Record

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The guinea pig has been chosen as a research model for otologic or neuropathic studies due to the relative ease of the cochlea, cochlear nerve, and vestibular nerve dissection. Little data have been reported on the normality of these nerves. The vestibular nerve is composed of the superior vestibular, inferior vestibular, and branch nerves. This study aimed to study the microscopic anatomy of the superior vestibular nerve (SVN) of guinea pigs using light microscopy and to search for normality patterns for use in experimental models in basic otologic research. We used eight male albino guinea pigs (Cavia porcellus, English strain), weighing between 400 and 500 g. After anesthetizing, the animals were perfused with a fixative solution of 2.5% glutaraldehyde. Dissection was performed by the access method to the temporal bone, coming to the rock and exposing the cochlea and vestibular nerve. The NVS fragments were removed, postfixed in osmium tetroxide, and embedded in the epoxy plastic resin Poly/Bed 812® (Polysciences Inc., Warrington, PA). Semi‐thin transverse serial sections (0.5 μm) were made using a microtome MT6000‐XL, RMC, Inc. and stained with toluidine blue. Morphology and morphometry were described and evaluated using the KS 400 application (Kontron 2.0, EchingBei, Munich, Germany) by macro, a computer program specially designed and developed for the study of the VIII nerve. The SVN was found to be devoid of epineurium, with only a thin conjunctive tissue layer. The myelin sheath of guinea pigs is relatively thin compared to the sensory and motor nerves found in mammals. The average fascicular area SVN was 0.19 ± 0.05 mm2, with the largest area found to be 0.24 mm2 and the lowest was 0.12 mm2. The average number of fibers was 5,753.00 ± 538 fibers. The density of myelinated fibers reached 32,316.08 ± 11,375.29 fibers/mm2. Its diameter ranged from 1.0 to 9 μm and its peak was 3 μm. The measured results confirm the results of another study, indicating that the methodology is appropriate and reproducible. These findings are important for the evaluation of injured nerves in experimental models of peripheral neuropathy and basic ear disease.

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“…Tremendous progress has been made in the development and validation of rodent models mimicking human CIDP (Table 1). The first chronic EAN models were developed in guinea pigs [74], rabbits [75], mice [76], and dark Agouti rats [77]. However, none of these models are in common use.…”

Section: Animal Modelsmentioning

confidence: 99%

“…Although the SAP model has provided some important information about potential immunopathogenic mechanisms of CIDP [79,80], one drawback for its use in translational therapy strategies studies is its late onset (20 weeks) and slow progression. Lewis rats P2(53-78) Acute [72] Lewis rats P0(180-199) Acute [66] Lewis rats PMP22 Acute [73] Juvenile guinea pigs BPN homogenate Chronic [74] Rabbits BPNM Chronic [75] Heterozygous KO (P0+/-) mice Inherited Chronic [76] Dark Agouti rats BPNM Chronic [77] B7-2 KO NOD mice Spontaneous Chronic [78] Lewis rats S-palm P0(180-199) Chronic [81] MBP: myelin basic protein; BPN: bovine peripheral nerve; BPNM: bovine peripheral nerve myelin; P0: protein zero; P2: protein two; PMP22: peripheral myelin protein-22; KO: knockout; NOD: non-obese diabetic; S palm P0(180-199): P0(180-199) peptide thiopalmitoylated at cysteine residue 181.…”

Section: Animal Modelsmentioning

confidence: 99%

CIDP: Current Treatments and Identification of Targets for Future Specific Therapeutic Intervention

Brun

Sèze

Muller

2022

Immuno

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Chronic inflammatory demyelinating polyneuropathy (CIDP) is an acquired immune-mediated inflammatory disorder of the peripheral nervous system. This clinically heterogeneous neurological disorder is closely related to Guillain–Barré syndrome and is considered the chronic counterpart of that acute disease. Currently available treatments are mostly empirical; they include corticosteroids, intravenous immunoglobulins, plasma exchange and chronic immunosuppressive agents, either alone or in combination. Recent advances in the understanding of the underlying pathogenic mechanisms in CIDP have brought a number of novel ways of possible intervention for use in CIDP. This review summarizes selected pre-clinical and clinical findings, highlights the importance of using adapted animal models to evaluate the efficacy of novel treatments, and proposes the outlines of future directions to ameliorate the conditions of patients with CIDP.

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Chronic experimental allergic neuritis (EAN) in juvenile guinea pigs: Immunological comparison with acute EAN in adult guinea pigs

Cited by 8 publications

References 26 publications

Inflammatory neuropathies: pathology, molecular markers and targets for specific therapeutic intervention

Inflammatory neuropathies: pathology, molecular markers and targets for specific therapeutic intervention

Morphological and morphometric study of the superior vestibular nerve trunk in guinea pigs

CIDP: Current Treatments and Identification of Targets for Future Specific Therapeutic Intervention

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