Gut bacteria can cause autoimmune disease – with comments from Dr. Gordon
By Linda on Dec 1, 2010 in F.I.G.H.T., Infections, Interesting Stories
Gut bacteria may cause autoimmune disease. We have all known this for some time but here is more research getting into how it happens.
My FIGHT program assumes that thanks to Monsanto and their BT (BACILLUS THERINGENSIS, i.e. the promised pesticide effect that caused farmers to buy into genetic modification of our food supply) along with continual exposure to antibiotics in our food supply causes me to take Kyodophilus 9 strain cap every day.
I also use my ACS 200 (Advanced Cellular Silver), which I know kills all fungi, molds, bacteria and virus so I always have to reimplant healthy bacteria a few hours later than my bid doses of ACS 200. I always feed the Kyodophilus organisms with Beyond Fiber, which includes stabilized rice bran (nature’s most nutrient dense food). It also has artichoke (FOS that causes too much gas), a fiber source of Lignans that helps provide the ideal mixture of soluble to insoluble fiber and long chain saccharides that helps support healthy intestinal flora and simultaneously helps drives out Candida continuously.
Garry F. Gordon MD,DO,MD(H)
President, Gordon Research Institute
www.gordonresearch.com
Link: http://www.the-scientist.com/article/display/57782/
Excerpt:
The finding
The trillions of microbes that reside in the human gut shape their host’s immune system—for better or for worse. In a mouse model of autoimmune arthritis, Diane Mathis from Harvard University and colleagues found that gut bacteria can provoke autoimmune disease in distant parts of the body—the joints.The surprise
When investigators raised transgenic mice (which develop the disease at 4 weeks of age) in germ-free conditions, the animals developed a milder version of the disease much later. Germ-free mice lack immune cells called T helper 17 cells (Th17), because these cells require the gut bacteria called segmented filamentous bacteria (SFB) to properly develop. When Mathis blocked IL-17—secreted by Th17 cells—in the normally raised mouse model, disease progression was also attenuated.The link
Mathis and colleagues showed that after SFB induced the accumulation of Th17 cells in the gut, the immune cells traveled to the spleen, where they helped activate antibody-producing B cells. Since the B cells in this mouse model produced self-attacking antibodies that initiated arthritis, the presence of IL-17 acted like a catalyst, quickening the disease. Though more work remains, “it is not hard to imagine the clinical relevance,” write Rochelle Marie Hinman and Faculty Member John Cambier.
