Endotoxin (lipopolysaccharide: LPS) infection due to bacterial translocation is intimately involved in the organ failure that occurs after highly invasive interventions such as extensive liver resection, and has attracted a great deal of interest. LPS that has translocated into portal blood binds to LPS-binding protein (LBP) and is transported to the monocytes and Kupffer cells in liver sinusoids where it is activated through the soluble CD14 that is present on their cell membranes or in blood plasma. Inflammatory cytokines such as TNF-alpha and IL-6 are produced and released by monocytes and Kupffer cells that have been activated by LPS-LBP complexes, and the endothelial cell of the sinusoids is damaged by these inflammatory cytokines. The original anticoagulant function of the damaged endothelial cells is reduced, and microcirculatory insufficiency is caused by the formation of microthrombi. It is important to understand this network mechanism and to prevent invasion, and attention has recently been focused on LBP and CD14 because of this point. The increase in LPS as a result of extensive liver resection, which is highly invasive, begins 3 hours after surgery, and peaks at 6 hours. LBP, however, is awaiting the entry of LPS, principally in the periportal hepatocytes. Its production peaks at 12 hours, and this is related to the excessive production of inflammatory cytokines have been produced, expression of LBP must be suppressed within 12 hours to inhibit this excessive reaction, and that will be the task of a future study.
|Number of pages||6|
|Journal||Nippon Geka Gakkai zasshi|
|Publication status||Published - 08-1998|
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