Seminar: The intestinal ecosystem as a modifier of autoimmune neuroinflammation
Abstract: The cause of multiple sclerosis (MS), a chronic autoimmune disease that targets the central nervous system, remains unknown. However, mounting evidence suggests that environmental factors, including infections and microbiome dysbiosis, are important risk factors for disease development. I have evaluated three distinct modalities by which the intestinal ecosystem influences immune system activation and the development of neuroinflammation in mouse models of MS.
First, a diet rich in a particular type of fibre, guar gum, delayed the onset of MS-like disease by dampening pro-inflammatory immune responses and inhibiting migration of immune cells into the central nervous system. Second, transfer of microbiota from aged human donors into mice promoted more severe MS-like disease than microbiota from young donors, and that treatment with young microbiota-derived metabolites reduced disease severity. Third, infection with an intestinal helminth skewed the immune response to prevent activation of pro-inflammatory immune cells during neuroinflammatory challenge, which ultimately promotes repair and remission of clinical symptoms during MS-like disease.
These areas of investigation highlight the diversity of environmental factors that contribute to development of autoimmune neuroinflammation, and identify novel mechanisms by which microbes, helminths, or their metabolic products could be harnessed for therapeutic advances.
If you are unable to make it in person, you can join us on Zoom:
Zoom: 92927 687268
ID: 687268
Seminar: The intestinal ecosystem as a modifier of autoimmune neuroinflammation
Abstract: The cause of multiple sclerosis (MS), a chronic autoimmune disease that targets the central nervous system, remains unknown. However, mounting evidence suggests that environmental factors, including infections and microbiome dysbiosis, are important risk factors for disease development. I have evaluated three distinct modalities by which the intestinal ecosystem influences immune system activation and the development of neuroinflammation in mouse models of MS.
First, a diet rich in a particular type of fibre, guar gum, delayed the onset of MS-like disease by dampening pro-inflammatory immune responses and inhibiting migration of immune cells into the central nervous system. Second, transfer of microbiota from aged human donors into mice promoted more severe MS-like disease than microbiota from young donors, and that treatment with young microbiota-derived metabolites reduced disease severity. Third, infection with an intestinal helminth skewed the immune response to prevent activation of pro-inflammatory immune cells during neuroinflammatory challenge, which ultimately promotes repair and remission of clinical symptoms during MS-like disease.
These areas of investigation highlight the diversity of environmental factors that contribute to development of autoimmune neuroinflammation, and identify novel mechanisms by which microbes, helminths, or their metabolic products could be harnessed for therapeutic advances.
If you are unable to make it in person, you can join us on Zoom:
Zoom: 92927 687268
ID: 687268