Gemini
Senior Member
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Acute infection can drive long-term immune & microbiota changes leading to chronic inflammatory disease in genetically pre-disposed individuals:
www.ncbi.nlm.nih.gov/pubmed/26764594/
This is a unified "hit- and-run" model involving genetic & metabolic signals, acute infection ultimately cleared, & "altered" microbiota-- in humans (it would appear)-- leading to chronic inflammatory disease.
A similar model has been discussed by ME/CFS researchers over the years, incl. Mady Horning.
Unfortunately the paper is behind a paywall. I'm curious about how prevalent the TLR1 genetic deficiency is; what specific inflammatory diseases the model applies to; and specifics about the treatments: gene deletion and targeted probiotics.
Wonder if the collaborators at the Univ of Chicago, Argonne Nat'l Laboratory, UCLA & UC-Davis might have any insights into the pathophysiology of ME/CFS?
www.ncbi.nlm.nih.gov/pubmed/26764594/
This is a unified "hit- and-run" model involving genetic & metabolic signals, acute infection ultimately cleared, & "altered" microbiota-- in humans (it would appear)-- leading to chronic inflammatory disease.
A similar model has been discussed by ME/CFS researchers over the years, incl. Mady Horning.
Unfortunately the paper is behind a paywall. I'm curious about how prevalent the TLR1 genetic deficiency is; what specific inflammatory diseases the model applies to; and specifics about the treatments: gene deletion and targeted probiotics.
Wonder if the collaborators at the Univ of Chicago, Argonne Nat'l Laboratory, UCLA & UC-Davis might have any insights into the pathophysiology of ME/CFS?