Absorption Of Endotoxin Research Articles

Effect of bile acids on the intestinal absorption of endotoxin in rats.

The absorption of tritium-labeled Escherichia coli O89 Westphal-type endotoxin from the peritoneal cavity of rats was diminished by bile by 23% and by sodium deoxycholate by 47%, respectively. Practically, there is no endotoxin absorption from the intestinal tract of normal rats. The bile duct of rats was chronically cannulated for experimental purposes. A significant amount of perorally administered endotoxin absorbed from the intestinal canal into the blood in the rats treated thus. Absorption was demonstrated by the lethal effect of endotoxin on rats previously hypersensitized by lead acetate, and by the radioactivities found in the blood samples. The intestinal absorption of endotoxin in rats, rendered bile-deficient, may be prevented by sodium deoxycholate. Supported by their experimental findings, we emphasize the important role of bile acids in the defense mechanism of the macroorganism against bacterial endotoxins.

INFLUENCE OF NEOMYCIN AND INGESTED ENDOTOXIN IN THE PATHOGENESIS OF CHOLINE DEFICIENCY CIRRHOSIS IN THE ADULT RAT.

Two groups of adult rats fed a choline-deficient diet supplemented with neomycin in their drinking water for 250 or 350 days were protected against the development of liver fibrosis and cirrhosis. At the termination of the study these animals weighed more than others not receiving neomycin. This difference in weight did not appear to be caused by a growth-promoting effect of neomycin but rather reflected the increased severity of liver disease and a resultant weight loss in animals not receiving neomycin. Protection by neomycin was cancelled when Salmonella typhosa endotoxin was added to the drinking water. It was concluded that the protective effect of neomycin was mediated by an alteration in the intestinal microflora resulting in a reduction in the numbers of organisms contributing to intraluminal endotoxin. In the presence of choline deficiency, absorption of intraluminal endotoxin may contribute to the development of fibrosis and cirrhosis.

On the absorption of bacterial endotoxin from the gastro-intestinal tract of the normal and shocked animal.

Coliform-free rabbits fed P(32) labeled E. coli 0111B(4) prior to the induction of experimental hemorrhagic shock were shown to have a substantial amount of the type-specific 0111B(4) antigen in the circulating blood, liver, and spleen, whereas normal rabbits fed the same amount of these bacteria and held under identical conditions, but not exposed to shock, have the antigen within the liver, and occasionally in the kidney, but not in the blood. That the antigen recovered from the blood and tissues was derived from this specific strain of bacteria was demonstrated by the use of the hemagglutination inhibition reaction, by the absence of cross-reacting antigens in appropriate control animals, and by agreement in the amount of antigen as estimated by two different technics. Transport of bacterial endotoxin across the intestinal membrane appears to be achieved primarily by passive diffusion. The accumulation of biologically active endotoxin in the blood and tissues of the shocked animal appears to be due to a reduction in the detoxifying potential of the reticulo-endothelial system, and not to a greater than normal absorption of endotoxin from the intestine. The absence of toxicity in the specific antigen extracted from normal liver demonstrates that the degradation of endotoxic potency can be achieved without altering the chemical integrity of the polysaccharide moiety of the molecule. The implications of the hypothesis that there is a continuous but fluctuating absorption of bacterial endotoxin from the intestine are briefly discussed, and the contribution of free circulating bacterial endotoxin of intestinal origin to the fate of the shocked animal is noted.

The leukocyte response in patients with sbigellosis

<h2>Summary</h2> A review of the white blood counts of a group of patients with shigellosis reveals counts ranging from 2,200 to 36,600 per cubic milliliter. There were a number of patients with definite leukopenia, a number with leukocytosis, and a number with perfectly normal white blood cell counts. The idea that the continued absorption of the Shigella endotoxin is capable of producing this picture of variation in leukocyte response is presented. The marked variation in the white blood cell count in patients with shigellosis makes the simple procedure of a white blood cell count of little use in the differential diagnosis of bacillary dysentery.