Liposaccharide constituting the outer membrane of Gram-negative bacteria.
Can cause the release of cytokines that induce hepatic stress and cholestasis.
Accelerates intestinal transit time.
Polymyxin B is an antibiotic with high affinity for endotoxin, but Polymyxin B hemoperfusion is not effective therapy in reducing mortality in septic shock.
Activates the host inflammatory response and mediates the clinical syndrome of sepsis.
Elevated endotoxin levels are independent of the causative organism isolated from the primary infection site.
The gastrointestinal tract can act as a reservoir of endotoxin in septic shock.
Endotoxin activity can be reliably measured and a high-level is associated with multiple organ failure and mortality in sepsis.
Therapies to neutralize endotoxin activity in clinical trials have yielded negative outcomes.