Speaker
Description
Multiple sclerosis (MS) is a multifactorial disorder, thus genetic disposition but also environmental factors are known to influence disease susceptibility and activity. This environmental modulation of central nervous system (CNS) autoimmunity can, inter alia, be mediated by the gut-brain axis, which is affected by nutritional components. Previous studies describe an influence of the poly-unsaturated fatty acid conjugated linoleic acid (CLA) in organ-specific autoimmunity such as rheumatoid arthritis and inflammatory bowel disease.
Hence, we want to characterize the immune-modulatory effects of dietary supplementation with CLA on the gut-brain axis in the context of MS. For this purpose, mice that spontaneously develop CNS autoimmunity were supplemented with CLA-rich diet. These mice showed an amelioration of disease severity accompanied by reduced CNS inflammation. Via flow cytometry, we characterized the effects on the gut-brain axis in more detail and determined changes in intestinal immune cell responses of CLA-fed mice, such as increased frequencies of regulatory T cells and affected myeloid cell activity in the intestine. Real-time measurement of oxygen consumption and extracellular acidification rate revealed an impaired energy metabolism in various immune cell subsets after CLA treatment in vitro. Besides direct effects on immune cells, CLA-rich diet alternated the intestinal microbiome composition, which can further modulate the gut-brain axis. Lactobacillus and Clostridium species are increased, whereas Prevotella and Blautia are reduced, which was contrary to the described microbiome of MS patients. To translate these findings into the human system, we performed a pilot study with 15 MS patients, which were daily supplemented with CLA over a period of six months. Similar to murine results, we determined immune-modulatory and some microbiota-changing effects in MS patients after CLA supplementation.
These data illustrate that dietary factors, such as CLA, play an important role in the modulation of CNS autoimmunity and further reflect a therapeutic potential to improve these autoimmune processes via the gut-brain axis.
