Abstract
Multiple sclerosis (MS) is an autoimmune neurological disease characterized by chronic inflammation of the central nervous system (CNS), leading to demyelination, axonal damage, and symptoms such as fatigue and disability. Although the cause of MS is not known, the infiltration of peripherally activated immune cells into the CNS has a key pathogenic role. Accumulating evidence supports an important role of diet and gut microbiota in immune-mediated diseases. Preclinical as well as clinical studies suggest a role for gut microbiota and dietary components in MS. Here, we review these recent studies on gut microbiota and dietary interventions in MS and its animal model experimental autoimmune encephalomyelitis. We also propose directions for future research.
Highlights
2.5 million people worldwide are affected by multiple sclerosis (MS), an autoimmune neurological disease of the central nervous system (CNS)
This review shows that many different microbial species and dietary interventions affect EAE disease expression and differences in gut microbiota between MS patients and healthy individuals may exist
Multiple small studies found that short-chain fatty acids (SCFA) producing bacteria are reduced in patients with MS, and the polysaccharide A (PSA) producing bacterium B. fragilis may be reduced B. fragilis is only found differently present in the gut by one study
Summary
2.5 million people worldwide are affected by multiple sclerosis (MS), an autoimmune neurological disease of the central nervous system (CNS). The cause of MS is not known, several lines of evidence point to a crucial pathogenic role of the immune system. Genome-wide association studies, neuropathological analyses, and successful therapy trials support the concept that peripheral interactions of environmental risk factors with MS-predisposing genetic factors elicit an autoimmune attack on the CNS causing the formation of lesions. Lesions are defined as usually sharply edged demyelinated areas within the white matter with a variable degree of inflammation, axonal damage, and gliosis. The presence of immune cells (T and B cells, macrophages) and immune molecules (antibodies, complement) supports the characterization of MS as an autoimmune-mediated inflammatory disease
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