Tracy Hampton, PhD
AMA. 2018; 320 (5) :. 429-430 doi: 10,1001 / Jama.2017.12863
Research Uncovers How Commensal Bacteria Contribute to Multiple Sclerosis
https://jamanetwork.com/journals/jama/a ... ct/2695647
A study recently published in Nature reveals that byproducts of microorganisms living in the gut may influence the progression of neurodegenerative diseases such as multiple sclerosis (MS) by controlling the interaction of 2 nonneuronal cell types: microglia and astrocytes. The findings may point to novel treatment strategies and suggest that inflammatory brain diseases could be dampened indirectly via the gut.
Since the vast majority of the immune system resides in the gut, this makes sense. My thought is that all disease and overall health is probably affected by the gut's bacterial makeup. A healthy gut, filled with overwhelmingly good bacteria, could contribute to overall better health and disease control.
Experts really have not studied this aspect of human health enough. This certainly warrants further study IMHO.
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So where the final conclusion that inflammatory brain disease could be dampened via the gut may be correct, it would seem these people haven’t understood or taken into consideration any of the basic underlying mechanisms.
How can you be so shortsighted? Sometimes, in my darkest dreams, I get the feeling that the discussion is carefully steered to circumvent the real issues….
Department of Neurology, Ruhr-University Bochum, Germany
Dietary Fatty Acids Directly Impact Central Nervous System Autoimmunity via the Small Intestine
Growing empirical evidence suggests that nutrition and bacterial metabolites might impact the systemic immune response in the context of disease and autoimmunity. We report that long-chain fatty acids (LCFAs) enhanced differentiation and proliferation of T helper 1 (Th1) and/or Th17 cells and impaired their intestinal sequestration via p38-MAPK pathway. Alternatively, dietary short-chain FAs (SCFAs) expanded gut T regulatory (Treg) cells by suppression of the JNK1 and p38 pathway. We used experimental autoimmune encephalomyelitis (EAE) as a model of T cell-mediated autoimmunity to show that LCFAs consistently decreased SCFAs in the gut and exacerbated disease by expanding pathogenic Th1 and/or Th17 cell populations in the small intestine. Treatment with SCFAs ameliorated EAE and reduced axonal damage via long-lasting imprinting on lamina-propria-derived Treg cells. These data demonstrate a direct dietary impact on intestinal-specific, and subsequently central nervous system-specific, Th cell responses in autoimmunity, and thus might have therapeutic implications for autoimmune diseases such as multiple sclerosis.
Hertie Senior Professor Group, Max Planck Institute of Neurobiology, Martinsried, Germany
Dietary non-fermentable fiber prevents autoimmune neurological disease by changing gut metabolic and immune status
The autoimmune neurological disease, Multiple Sclerosis (MS), have increased at alarming rates in the Western society over the last few decades. While there are numerous efforts to develop novel treatment approaches, there is an unmet need to identify preventive strategies. We explored whether central nervous system (CNS) autoimmunity can be prevented through dietary manipulation using a spontaneous autoimmune encephalomyelitis mouse model. We report that the nutritional supplementation of non-fermentable fiber, common components of a vegetarian diet, in early adult life, prevents autoimmune disease. Dietary non-fermentable fiber alters the composition of the gut microbiota and metabolic profile with an increase in the abundance of long-chain fatty acids. Immune assays revealed that cecal extracts and a long chain fatty acid but not cecal lysates promoted autoimmune suppressive TH2 immune responses, demonstrating that non-fermentable fiber-induced metabolic changes account for the beneficial effects. Overall, these findings identify a non-invasive dietary strategy to prevent CNS autoimmunity and warrants a focus on nutritional approaches in human MS.
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