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Abstract
Male Lewis rats (6 weeks-old) were submitted to a calorie restriction equivalent to 33% or 66% of food restriction. Fifteen days later, groups of 7 animals were injected with complete Freund's adjuvant plus spinal cord homogenate (SCH) to induce experimental allergic encephalomyelitis (EAE) or with complete Freund's adjuvant alone. EAE was defined solely on clinical grounds. Rats were assessed daily for clinical signs of EAE and were killed on day 15 after immunization. Both diet and SCH injection diminished body weight significantly. In contrast to rats receiving a normal diet or a 33% calorie-restricted diet, rats subjected to severe calorie restriction did not exhibit clinical signs of EAE. Concomitantly with the lack of disease manifestation, 66% of calorie-restricted rats injected with SCH showed significantly less splenic and lymph node mitogenic response to concanavalin A (Con A) and a higher splenic response to lipopolysaccharide. Fewer splenic, lymph node and thymic CD4+ cells, greater numbers of splenic and lymph node CD8+ and CD4+- CD8+ cells, and fewer splenic T, B and T-B cells, and lymph node and thymic B and T-B cells were observed. There was impaired interferon (IFN)-γ production occurred in the three examined tissues. The results are compatible with the view that the acute phase of EAE can be curtailed by severe calorie restriction, presumably through impaired IFN-γ production.
Highlights
Multiple sclerosis (MS) is an autoimmune disease that results in demyelination of axonal tracts in the CNS causing a wide range of neurological symptoms [1]
Rats subjected to the normal diet or to a 33% calorie restriction exhibited clinical signs of the disease, starting on day 12 after spinal cord homogenate (SCH) injection whereas, a 66%-calorie restriction effectively suppressed the course of EAE in Lewis rats (Fig. 1, lower panel)
Data shown as mean ± SEM (n = 7 rats/group)
Summary
Multiple sclerosis (MS) is an autoimmune disease that results in demyelination of axonal tracts in the CNS causing a wide range of neurological symptoms [1]. Epidemiological studies suggest that unidentified environmental factors contribute to the etiology of MS [2,3] and diet is a commonly postulated factor because strong associations have been observed between increased MS prevalence and diets high in meat and dairy products and low in fish [1,4,5,6] These epidemiological findings have provided a rationale for a number of clinical trials aimed to establish beneficial effect of dietary interventions in MS, with heterogeneous results [1]. Experimental allergic encephalomyelitis (EAE) animal models share many characteristics of MS [10] This includes an "activation phase" where antigenpresenting cells process the immunized antigen, migrate to the lymph nodes and present immunodominant peptides to naïve T-cells; and an "effector phase" where CD4+ T-cells that recognize antigen proliferate and cross the blood-brain barrier to lead an inflammatory attack that results in demyelinated lesions. The T helper 1 (Th1) subset of T-cells has been implicated in the induction of EAE
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