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david.crichton · Joined: 02 May 2008 Posts: 83

Enhanced TNF-alpha secretion is associated more strongly with CD than UC, IBS or controls and even more strongly associated with MAP positive CD patients.

Maybe this strengthens the argument that anti-TNF-alpha biologics treat MAP infections and not just inflammatory molecules? See a quick explanation for how it might be possible that anti-TNF-alpha biologics are causing cell death of those cells that contain MAP: http://www.nulltone.com/?page_id=30 Quoting Nulltone.com - "Anti-TNF antibodies such as Remicade and Humira are now believed to trigger apoptosis (cell death) in immune cells, specifically macrophages. Macrophages are known to be the source of inflammatory cytokines in Crohn’s disease. The therapeutic effect of TNF-alpha antibodies for Crohn’s was originally thought to be from neutralizing TNF-alpha as it was traveling outside of the macrophage. Several new studies show that Remicade and Humira’s therapeutic effect is likely due to the binding of TNF-alpha while it is still bound to the membrane of macrophages, and this triggers apoptosis (cell death) in these immune cells. Macrophages in cattle with Johne’s disease are the immune cells that contain Map, so one could see how a drug that destorys those cells would disrupt Map infection and Map immune dysregulation."

Exploited · Joined: 24 Jan 2008 Posts: 42

Very interesting!