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Steve E. Calvano, PhD
New Brunswick, NJ

Arch Surg. 2004;139:655.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

In 1892 Robert Koch's coworker, Richard Pfeiffer, first described bacterial endotoxin as a moiety distinct from secreted, heat-labile exotoxins. Now, some 112 years later, we have extensive knowledge of the mechanism of action of endotoxin, although, amazingly, some pieces of what turned out to be a complex puzzle have only been elucidated in the past few years. Although it had been known since the early 1990s that the cell surface receptor for endotoxin was a protein called CD14, the mechanism by which this receptor signaled the presence of endotoxin remained enigmatic because CD14 lacks a cytoplasmic tail. The solution to this puzzle awaited the discovery of the toll-like receptor 4, a second endotoxin-binding receptor. Yet, many of the sequelae of endotoxin are not via a direct effect on cellular physiology but rather caused by amplified cascades of downstream events that are initiated by endotoxin. Probably the . . . [Full Text of this Article]

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