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        <title>Article Comments - 'Is inflammaging an auto[innate]immunity subclinical syndrome?'</title>
        <link>http://www.immunityageing.com/content/3/1/12/comments</link>
        <description>The latest comments on the article 'Is inflammaging an auto[innate]immunity subclinical syndrome?'</description>
        <dc:date>2006-12-19T00:00:00Z</dc:date>
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        <item rdf:about="http://www.immunityageing.com/content/3/1/12/comments#250537">
        <title>We have a lot to learn about 'diseases of the aging'</title>
        <link>http://www.immunityageing.com/content/3/1/12/comments#250537</link>
        <description>&lt;p&gt;In 2004 we described how the chronic inflammatory disease, sarcoidosis, is caused by a life-long accumulation of intra-phagocytic bacterial pathogens[1]. We recently published an update[2], reporting that many chronic inflammatory diseases result from a similar pathogenesis. Our Phase 2 clinical trial has already been demonstrating recovery from some of the diseases of aging, particularly arthritis, osteopenia, and even diabetes[3].&lt;/p&gt;&lt;p&gt;Interestingly, those patients who have recovered from terminal inflammatory conditions, such as sarcoidosis and rheumatoid arthritis, report that recovery feels like &quot;being 20 years younger.&quot; We are also observing that the body has an amazing ability to regenerate after inflammatory damage which is currently considered to be &apos;permanent&apos; (eg, fibrosis and peripheral neuropathy). Clearly we still have a lot to learn about the processes which society categorizes as &apos;aging&apos;.&lt;/p&gt;&lt;p&gt;Our research points towards Th1 inflammation, the innate immune response to intraphagocytic pathogens, as being the cause of so many &quot;disease of the aging,&quot; ranging from atherosclerosis, cardiomyopathy and arthritis through to many neurological conditions, and even to dementia. &lt;/p&gt;&lt;p&gt;We have shown much chronic inflammation results from the body&apos;s innate immune response, and we agree it seems likely that &apos;Inflammaging&apos; may also result from this same pathogenesis.&lt;/p&gt;&lt;p&gt; &lt;/p&gt;&lt;p&gt;References:&lt;/p&gt;&lt;p&gt;1. Marshall TG, Marshall FE: Sarcoidosis succumbs to antibiotics - implications for autoimmune disease. Autoimmunity Reviews,2004; 3(4):295-3001&lt;/p&gt;&lt;p&gt;2. Marshall TG: VDR Nuclear Receptor Competence is the Key to Recovery from Chronic Inflammatory and Autoimmune Disease. Abstract presentation, Days of molecular medicine, 2006.&lt;/p&gt;&lt;p&gt;Copy available from URL http://autoimmunityresearch.org/karolinska-handout.pdf&lt;/p&gt;&lt;p&gt;3.  Waterhouse JC, Marshall TG, Fenter B, Mangin M, Blaney G: High levels of active 1,25-dihydroxyvitamin D despite low levels of the 25-hydroxyvitamin D precursor - Implications of dysregulated vitamin D for disgnosis and treatment of Chronic Disease. In Vitamin D: New Research. Volume 1. Edited by: Stoltz VD. New York: Nova Science Publishers; 2006. ISBN: 1-60021-000-7&lt;/p&gt;&lt;p&gt;4. Marshall TG: Are statins analogs of vitamin D?. Correspondence to Grimes, DS. The Lancet 2006; 368:1234 doi:10.1016/S0140-6736(06)69509-3&lt;/p&gt;&lt;p&gt;Copy available from URL http://www.thelancet.com/journals/lancet/article/PIIS0140673606695093/fulltext&lt;/p&gt;&lt;p&gt;5. Marshall TG: A New Approach to Treating Intraphagocytic CWD Bacterial Pathogens in Sarcoidosis, CFS, Lyme and other Inflammatory Diseases. American Academy of Environmental Medicine; 2006, Plenary Sessions Syllabus, 41st Annual Meeting.&lt;/p&gt;&lt;p&gt;Copy available from URL http://autoimmunityresearch.org/aaem_2006.ram&lt;/p&gt;&lt;p&gt;6. Marshall TG: Molecular genomics offers new insight into the exact mechanism of action of common drugs - ARBs, Statins, and Corticosteroids. FDA CDER Visiting Professor presentation, FDA Biosciences Library, Accession QH447.M27 2006&lt;/p&gt;&lt;p&gt;Copy available from URL http://autoimmunityresearch.org/fda-visiting-professor-7mar06.ram&lt;/p&gt;&lt;p&gt;7. Marshall TG, Lee RE, Marshall FE: Common angiotensin receptor blockers may directly modulate the immune system via VDR, PPAR and CCR2b. Theor Biol Med Model. 2006 Jan 10;3(1):1. Available from URL http://www.tbiomed.com/content/3/1/1&lt;/p&gt;&lt;p&gt;8.Marshall TG, Fenter BJ, Marshall FE: Antibacterial Therapy Induces Remission in Sarcoidosis (in English). JOIMR 2005;3(1):2 Available from URL http://www.joimr.org/phorum/read.php?f=2&amp;#38;i=107&amp;#38;t=107&lt;/p&gt;</description>
                <dc:creator>Trevor Marshall</dc:creator>
                <dc:date>2006-12-19T00:00:00Z</dc:date>
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