The most powerful sepsis trigger.
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Endotoxin, also referred to as Lipopolysaccharide (LPS), a component of the cell wall of Gram negative bacteria, is one of the main triggers of the pathogenesis of septic shock and multiple organ failure. Its entry into the bloodstream stimulates monocytes/macrophages that, once activated, produce and release cytokines such as TNF and IL-6, nitric oxide and other mediators that induce systemic inflammation, endothelial damage, hypotension (shock), and multiple organ dysfunction.
Endotoxin & Polymyxin B
Over the past decade, it is has been recognized that removing or neutralizing endotoxin from the bloodstream is an effective therapeutic tool in the treatment of septic shock. Among the various strategies studied to eliminate endotoxin, Polymyxin-B hemoperfusion has been the most effective in blocking the toxic effects of endotoxin by virtue of its electrochemical affinity with Lipid A (common to all species of endotoxin). However, systemic use of Polymyxin B is limited by severe nephro- and neurotoxicity.
The interaction between Polymyxin B and Lipid A of endotoxin is governed primarily by forces which include:
I• Ionic: guides the formation of the link/bond;
• Hydrophobic: breaks the spatial order of the acyl chains of LPS and neutralizes the toxicity, transforming LPS and Polymyxin B into a single unimolecular compound.
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