Endotoxin, reticuloendothelial function, and liver injury.
The concept that relates intestinal bacteria and their toxins as a common pathway of liver injury by toxic agents has interested investigators for a long period. Recently, a number of studies in experimental animals and in patients with liver disease support this contention, and are reviewed. Evidence is presented to suggest that: (a) function of the sinusoidal cells is critical to integrity of the hepatocyte; (b) damage to these lining cells by several agents may be the initial injury leading to decreased ability of the liver to detoxify endotoxin (LPS); (c) following this primary injury to Kupffer and endothelial cells, LPS causes damage at amounts which are ordinarily innocuous and may represent a final pathway of liver necrosis; (d) "spillover" of LPS may lead to systemic manifestations of liver disease, and (e) modification of endotoxin toxicity or absorption may protect against several acute and chronic liver injuries.
D000818:Animals; D002252:Carbon Tetrachloride Poisoning / Q000503:physiopathology; D004731:Endotoxins / Q000494:pharmacology*; D006801:Humans; D007422:Intestines / Q000382:microbiology; D007728:Kupffer Cells / Q000502:physiology; D008070:Lipopolysaccharides / Q000494:pharmacology; D008099:Liver / Q000473:pathology / Q000502:physiology*; D008107:Liver Diseases / Q000209:etiology / Q000503:physiopathology; D051379:Mice; D012157:Mononuclear Phagocyte System / Q000502:physiology*; D009336:Necrosis; D051381:Rats
D004731:Endotoxins; D008070:Lipopolysaccharides