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--- home:publications:proal_autoimmunity_2010 [06.15.2010] – marysue
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 Well, it may also not be by accident that the uniqueness with which a patients' autoimmune symptoms develop parallels the incredible diversity of the pathogens that can persist in the human body. The following wheel shows how truly related chronic diseases are. Each “spoke” on the wheel represents a published study that's shown a significant statistical relationship between patients suffering from one disease and the next. And that is a lot of comorbidity and a lot of symptom overlap.
 ====#15 Select bacterial genera detected in commonly smoked cigarettes====
-So, where do we pick up these pathogens? They're everywhere! They're passed from mother to child during pregnancy, from father to child in sperm, through familial contact, they're in injectable medicines, they're in donated blood. There are many vectors. Consider for interest though, a study came out recently.  This is a group that tested for total bacterial diversity of four brands of cigarettes.(({{pubmed>long:20064769}})) And they found fifteen different classes of bacteria and a wide range of pathogenic microorganisms in every single cigarette tested – even the Kools!
+So, where do we pick up these pathogens? They're everywhere! They're passed from mother to child during pregnancy, from father to child in the sperm, obviously through familial contact, they're in injectable medicines, they're in donated blood. There are many vectors. Consider for interest though, I thought this was interesting, a study came out recently - this is a group that tested for total bacterial diversity in four brands of cigarettes.(({{pubmed>long:20064769}})) And they found fifteen different classes of bacteria and a wide range of pathogenic microorganisms in every single cigarette tested – even the Kools!
+Finally, and I want to stress this, the model of successive infection has great implications for the way autoimmune disease should be treated. If microbes - both bacterial and viral - are driving the autoimmune disease state, then treatments that suppress the immune response can at best succeed in achieving short-term palliation. They offer temporary relief by slowing the inflammation that would otherwise be generated if the immune system were actually targeting the pathogens. But instead the pathogens remain alive and they're able to proliferate - and they cause the person to become sicker over the long term.
-Finally, and I want to stress this, the model of successive infection has great implications for the way autoimmune disease should be treated. If microbes - both bacterial and viral - are driving the autoimmune disease state, then treatments that suppress the immune response can best succeed at offering short-term palliation. They offer temporary relief by slowing the inflammation that would otherwise be generated if the immune system were actually targeting the pathogens. But instead the pathogens remain alive and they're able to proliferate - and they cause the person to become sicker over the long term.
+Well, this being said, I work with the non-profit Autoimmunity Research Foundation and we, over the last six years have been working with a treatment for autoimmune disease that stimulates rather than suppresses the immune response in autoimmune disease. And, key to the treatment is the use of a VDR agonist which turns on - returns on - those components of the innate immune system that I described before that were so important.  And, the results of the treatment thus far are really interesting, at least in my opinion, because we have patients who are not only feeling better, but presenting with objective markers indicating significant improvement.  My colleagues will be talking more about the treatment in the vitamin D session and translational medicine session in hall C, I think, at two - and I really, highly encourage you to attend!
-Well, this being said, I work with the non-profit Autoimmunity Research Foundation and we, over the last six years have been working with a treatment for autoimmune disease that stimulates rather than suppresses the immune response in autoimmune disease. And, key to the treatment is the use of a VDR agonist which turns on - returns on - those key components of the innate immune system that I described before that were so important.  And, the results of the treatment thus far are, at least in my opinion, fascinating, because we have patients who are not only feeling better, but present with objective markers indicating significant improvement.  My colleagues will be talking more about the treatment in the vitamin D session and translational medicine session in hall C, I think, at 2 - and I really, highly encourage you to attend!
 ====#16 "Don't palliate, stimulate!"====

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