INDUCTION OF EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS IN RATS WITHOUT THE AID OF ADJUVANT<sup>*</sup>

Levine, Seymour; Wenk, Eugene J.

doi:10.1111/j.1749-6632.1965.tb20204.x

Cited by 39 publications

(4 citation statements)

References 30 publications

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“…Pioneering work by Levine and Wenk, using guinea pig MBP mixed with CFA, additionally injected with pertussis toxin, induced hyperacute EAE characterized by massive inflammation that correlated with clinical signs (Levine & Wenk, ). Later, pertussis toxin was excluded from adjuvants used to afflict animals.…”

Section: Selection Of Animals In Eaementioning

confidence: 99%

Animal models of multiple sclerosis: Focus on experimental autoimmune encephalomyelitis

Bjelobaba

Begović-Kuprešanin

Peković

et al. 2018

J of Neuroscience Research

133

102

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Multiple sclerosis (MS) is a chronic, progressive disorder of the central nervous system (CNS) that affects more than two million people worldwide. Several animal models resemble MS pathology; the most employed are experimental autoimmune encephalomyelitis (EAE) and toxin- and/or virus-induced demyelination. In this review we will summarize our knowledge on the utility of different animal models in MS research. Although animal models cannot replicate the complexity and heterogeneity of the MS pathology, they have proved to be useful for the development of several drugs approved for treatment of MS patients. This review focuses on EAE because it represents both clinical and pathological features of MS. During the past decades, EAE has been effective in illuminating various pathological processes that occur during MS, including inflammation, CNS penetration, demyelination, axonopathy, and neuron loss mediated by immune cells.

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Section: Selection Of Animals In Eaementioning

confidence: 99%

Animal models of multiple sclerosis: Focus on experimental autoimmune encephalomyelitis

Bjelobaba

Begović-Kuprešanin

Peković

et al. 2018

J of Neuroscience Research

133

102

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“…Lewis rats are susceptible to several (inducible) autoimmune diseases including uveitis, 29 valvulitis, 32,75 encephalomyelitis, 63,64 and inflammatory arthritis, 38,58,110,120 due to genetic alterations that are characterized by reactivity of the HPA axis. This alteration results in an abnormally higher and prolonged release of glucocorticoids than in other rat strains, 33,109 which thus makes the Lewis rat prone to infectious diseases including periodontitis.…”

Section: Discussionmentioning

confidence: 99%

“…We chose Lewis rats because of their well-characterized genetic susceptibility to various inducible T-cell mediated autoimmune diseases. 20,29,32,38,58,63,64,67,73,75,98,119,120 In addition, Th1 and Th17 effector responses associated with the development of autoimmune diseases are unique in Lewis rats. 73,74,109,118 Furthermore, accentuated Th1 responses and imbalances between Th17 and regulatory T cells have been shown to contribute to uveitis 20,118 and encephalomyelitis 73 in Lewis rats.…”

mentioning

confidence: 99%

Diet-induced Generalized Periodontitis in Lewis Rats

Messer

Kipp

et al. 2019

comp med

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Periodontitis is an important public health concern worldwide. Because rodents from the genus Rattus are resistant to spontaneous periodontitis, experimental periodontitis must be initiated by mechanical procedures and interventions. Due to their exacerbated Th1 response and imbalanced Th17 regulatory T-cell responses, Lewis rats are highly susceptible to inducible inflammatory and autoimmune diseases. We hypothesized that feeding Lewis rats a diet high in sucrose and casein (HSC) would alter the oral microenvironment and induce inflammation and the development of periodontitis lesions without mechanical intervention. A baseline group (BSL, n = 8) was euthanized at age 6 wk. Beginning at 6 wk of age, 2 groups of Lewis rats were fed standard (STD, n = 12) or HSC (n = 20) chow and euthanized at 29 wk of age. We evaluated the degree of periodontitis through histology and μCT of maxillae and mandibles. The HSC-induced inflammatory response of periodontal tissues was assessed by using immunohistochemistry. Gene expression analysis of inflammatory cytokines associated with Th1 and Th17 responses, innate immunity cytokines, and tissue damage in response to bacteria were assessed also. The potential systemic effects of HSC diet were evaluated by assessing body composition and bone densitometry endpoints; serum leptin and insulin concentrations; and gene expression of inflammatory cytokines in the liver. Placing Lewis rats on HSC diet for 24 wk induced a host Th1-immune response in periodontal tissues and mild to moderate, generalized periodontitis characterized by inflammatory cell infiltration (predominantly T cells and macrophages), osteoclast resorption of alveolar bone, and hyperplasia and migration of the gingival epithelium. HSC-fed Lewis rats developed periodontitis without mechanical intervention in the oral cavity and in the absence of any noteworthy metabolic abnormalities. Consequently, the rat model we described here may be a promising approach for modeling mild to moderate periodontitis that is similar in presentation to the human disease.

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“…The list of actively induced EAE variants in experimental animals without adjuvant or with IFA is provided in Table 1 . Importantly, the idea of using CFA-free animal models in the study of CNS autoimmunity is not novel, having been proposed by pioneers in the field, Levine and Wenk, some 60 years ago ( 65 ). These authors were able to show that EAE can be induced by intracutaneous injection of neural tissue homogenates without adjuvant in various strains of rats, with Lewis rats being the most susceptible.…”

Section: Eae Models Without Cfamentioning

confidence: 99%

Complete Freund’s adjuvant as a confounding factor in multiple sclerosis research

Lazarević,

Stanisavljević,

Nikolovski

et al. 2024

Front. Immunol.

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Complete Freund’s adjuvant (CFA) is used as a standard adjuvant for the induction of experimental autoimmune encephalomyelitis (EAE), the most commonly used animal model in multiple sclerosis studies. Still, CFA induces glial activation and neuroinflammation on its own and provokes pain. In addition, as CFA contains Mycobacteria, an immune response against bacterial antigens is induced in parallel to the response against central nervous system antigens. Thus, CFA can be considered as a confounding factor in multiple sclerosis–related studies performed on EAE. Here, we discuss the effects of CFA in EAE in detail and present EAE variants induced in experimental animals without the use of CFA. We put forward CFA-free EAE variants as valuable tools for studying multiple sclerosis pathogenesis and therapeutic approaches.

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INDUCTION OF EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS IN RATS WITHOUT THE AID OF ADJUVANT^*

Cited by 39 publications

References 30 publications

Animal models of multiple sclerosis: Focus on experimental autoimmune encephalomyelitis

Animal models of multiple sclerosis: Focus on experimental autoimmune encephalomyelitis

Diet-induced Generalized Periodontitis in Lewis Rats

Complete Freund’s adjuvant as a confounding factor in multiple sclerosis research

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INDUCTION OF EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS IN RATS WITHOUT THE AID OF ADJUVANT*

Cited by 39 publications

References 30 publications

Animal models of multiple sclerosis: Focus on experimental autoimmune encephalomyelitis

Animal models of multiple sclerosis: Focus on experimental autoimmune encephalomyelitis

Diet-induced Generalized Periodontitis in Lewis Rats

Complete Freund’s adjuvant as a confounding factor in multiple sclerosis research

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INDUCTION OF EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS IN RATS WITHOUT THE AID OF ADJUVANT^*