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At least 19 recordsLinked to original sources

PubMed1978

Endotoxin receptor site. II. Specificity of endotoxin receptor of platelets and sensitivity to endotoxin in vivo.

The biological specificity of the endotoxin receptor on platelet membranes was examined. The binding indices of platelets in experimental endotoxemia which was induced by intravenous administration of endotoxin (Lipopolysaccharide of E. coli, Difco) to rabbits were found to be 30% of the control at 60 min after the injection. The result suggests that the endotoxin receptor of platelets was already occupied. The binding indices of human platelets were measured after pretreatment with pharmacologically active substances which were assumed to effect platelet activity. The binding of LPS to platelets showed competitive inhibition at pharmacologically effective doses, but other substances merely inhibited platelet activity. One interpretation is that there is a common receptor on platelet cell membranes for lipopolysaccharide of E. coli and endotoxin. The sensitivity to endotoxin in vivo and binding indices of platelets were examined in rabbits and guinea pigs since their response to endotoxin is almost opposite with regard to sensitivity. The binding indices of platelets from rabbits and guinea pigs showed a positive correlation with the endotoxin sensitivity. Those findings indicate that platelets play a key role in vivo in the clinical course of endotoxemia.

Age Factors↗

PubMed1976

Cholestatic effects of Escherichia coli endotoxin endotoxin on the isolated perfused rat liver.

The effects of Escherichia coli endotoxin on the function of the ex vivo perfused rat liver were examined in order to investigate the possible role of circulating endotoxin in the pathogenesis of cholestatic jaundice observed in humans with gram-negative bacterial infections. Endotoxin led to a dose-dependent impairment of bile flow and of sulfobromophthalein (BSP) excretion. The demonstration that indocyanine green excretion was also significantly decreased by endotoxin suggests that the impaired dye excretion was not due to an inhibition of BSP conjugation in the hepatocyte. Analysis of the kinetic data suggested that the effects of endotoxin were on the excretory mechanisms of the hepatocyte. These effects did not seem attributable to endotoxin-mediated changes in perfusate flow since a mechanical reduction in perfusate flow caused no decrease in the excretion of bile or BSP. The results of the present study provide supportive evidence for the hypothesis that circulating endotoxin can adversely affect hepatic function and may contribute to the production of intrahepatic cholestasis seen during bacterial infection. Hepatocyte injury by endotoxin, as judged by the leakage of enzymes from hepatocyte suspensions or from the perfused rat liver, could not be demonstrated.

Animals↗

PubMed1977

Anaphylactic reactions to endotoxin in guinea-pig tissues: relationship to endotoxin toxicity.

1 A lipopolysaccharide extract of Escherichia coli 026:B6 cells (026:B6(B) endotoxin) was shown to be toxic to normal adult guinea-pigs. 2 The agent had no action on isolated preparations of ileum and heart taken from normal adult guinea-pigs. 3 Ileal segments from animals actively immunized against 026:B6(B) endotoxin showed dose-dependent contractions when exposed to endotoxin. Desensitization phenomena were demonstrated. 4 Reactivity of 026:B6(B) endotoxin was transferred to isolated preparations of ileum and heart from normal animals by passive transfer of immune serum. 5 Tissue responses to 026:B6(B) were associated with release of ileal spasmogen into the bath medium. Mepyramine blocked the effects of this spasmogen at bath concentrations which caused little change in ileal responses to carbachol. 6 It is concluded that E. coli endotoxin can elicit anaphylactic reactions, and that this process may potentiate endotoxin toxicity in sensitized animals. However, endotoxin toxicity in guinea-pigs does not appear to depend on this kind of allergic process.

Anaphylaxis↗

PubMed1977

Biological activities of tritiated endotoxins: correlation of the Limulus lysate assay with rabbit pyrogen and complement-activation assays for endotoxin.

Tritiated endotoxins were prepared by three different methods. The biological activities of the tritiated endotoxins were determined by the Limulus amebocyte lysate assay, a rabbit pyrogen assay, and a complement-activation assay and were compared to native, unlabeled endotoxin. All three tritiated endotoxin preparations manifested adequate biological activity in each of the three assay systems, and all three assays ranked the biological activity of the different endotoxin preparations in the same order. Endotoxin tritiated by the Wilzbach procedure retained most of its biological activity and also had the highest specific radioactivity. The good correlation between the Limulus lysate, rabbit pyrogen, and complement-activation assays suggests that the same active site of the endotoxin molecule is identified by the three different assays.

Animals↗

PubMed1978

Rat macrophage-mediated toxicity to cancer cells; effect of endotoxins and endotoxin inhibitors contained in culture media.

The cytotoxic effect of normal or BCG-activated rat macrophages on a syngeneic line of cancer cells was compared in media containing rat or bovine sera. Normal macrophages were usually cytotoxic to cancer cells in fetal or newborn bovine serum; however, they enhanced cancer cell growth in normal rat serum. BCG- activated macrophages were toxic to cancer cells regardless of the serum used in the assay. Many cell culture media or sera obtained commercially were found to be contaminated by bacterial endotoxins. When endotoxin-free reagents were used in the toxicity assay, different results were observed: normal macrophages were not cytotoxic, but rather, they often enhanced cell growth even in fetal bovine serum; toxicity of activated macrophages was significantly reduced in normal rat serum. These results suggest that endotoxin and endotoxin inhibitors play a role in the modulation of macrophage-mediated cytotoxicity. These results emphasize the importance of monitoring endotoxin contamination in cell culture reagents used in assays involving macrophages.

Animals↗

PubMed1978

Experiments on prevention of the endotoxin-abortifacient effect by radiodetoxified endotoxin pretreatment in rats.

Endotoxemia has been induced in pregnant rats by intravenous injection of 1 mg Escherichia coli endotoxin which resulted in intrauterine death and abortion of fetuses in 24 h. The abortifacient effect of endotoxin was prevented in 90% by 200 microgram radiodetoxified endotoxin, injected intravenously 24 h earlier. The authors suppose that the radiodetoxified endotoxin can be a good tool also in the prevention of human septic (endotoxin) shock in pregnancy.

Abortifacient Agents↗

PubMed1976

Measurement of endotoxin. I. Fundamental studies of radioimmunoassay of endotoxin.

A method for estimating endotoxin by radioimmunoassay was recently introduced. The present paper describes improvements in the speed and sensitivity on this endotoxin measurement. Antigen was purified from E. coli O111: B4 (B) lipopolysaccharide by centrifugation and dialysis. Purified anti-endotoxin antibody was prepared from immunized rabbit serum. A radioimmunoassay system was established with the antigen and antibody. Dextran-coated charcoal was used to separate the antibody-bound antigen from free antigen. Experimental studies were also performed on possible factors related to the antigen-antibody reaction. Accurate measurements on quantities as low as 100 pg/ml (10ng/ml in the plasma) were performed by the dextran-coated charcoal method, and the reaction time was reduced to 2 hr at 4 degrees C. This new method does not require strict sterilization or aseptic handling, and therefore is quite practical for quantitative measurements of endotoxin.

Animals↗

PubMed1978

Endotoxin receptor site. I. Binding of endotoxin to platelets.

Binding of bacterial endotoxin to platelets, erythrocytes, lymphocytes and granulocytes was examined by using diffusion dialysis. Platelets, erythrocytes, lymphocytes and granulocytes were fractionated from normal human blood and the binding of endotoxin (LPS: Lipopolysaccharide of E. coli) to each cell fraction was measured at 4 degrees C and the binding efficiency was expressed as a binding index (%d4degreesC +/- SD). The binding index for each cell fraction was as follows; 10.2 +/- 1.6 for platelets, 1.0 +/- 0.9 for erythrocytes, 4.3 +/- 1.6 for lymphocytes and 10.0 +/- 1.5 for granulocytes (n = 11) respectively. Since a platelet possesses a small cell surface area compared with other cells, it was clear that the endotoxin bound preferentially to platelets in vitro. The binding mechanism to the platelet cell surface was suggested to be direct binding of endotoxin to the receptor on platelet cell membrane rather than through an immunologically activated mechanism.

Blood Platelets↗

PubMed1977

Effect of endotoxin-induced shock on the reticuloendothelial system. Phagocytic activity and DNA-synthesis of reticuloendothelial cells following endotoxin treatment.

There was a marked decrease in the RES phagocytic activity during the first 12 hours after injection of high concentrations of endotoxin in rats. Phagocytic activity then increased considerably, reaching maximum values on days 3 to 5 and it was still higher than in control animals 20 days later. Parallel studies on 3H thymidine incorporation showed a significant increase in the rate of DNA-synthesis of reticulum cells of the liver during the 5 days period following endotoxin injection. Peak values were obtained on day 2 when the number of labelled cell were 50 times higher than in the controls. A likely reason for the increased DNA-synthesis is a repair of RES following endotoxin induced damage but it may also represent an endotoxin induced proliferation of reticulum cells that may at least partly account for the enhanced phagocytic activity.

Animals↗

PubMed1977

Inhibition of Na+, K+-adenosinetriphosphatase by endotoxin: a possible mechanism for endotoxin-induced cholestasis.

Cholestatic jaundice is one complication of nonhepatic gram-negative bacterial infection. The endotoxin of Escherichia coli has been reported to cause cholestasis by inhibiting the bile salt-independent fraction (BSIF) of bile in the perfused rat liver. Accordingly, the effects of lipopolysaccharides (LPS) of E. coli and Salmonella enteritidis on the Na+, K+-adenosinetriphosphatase (ATPase) in canalicular-enriched plasma membranes of rate liver were examined. At 20 microgram/ml, both endotoxins inhibited this enzyme by approximately 40%. Maximal inhibition (70%-80%) occurred at concentrations of greater than or equal to 120 microgram/ml. The LPS of neither organism exerted any effect on the activity of Mg++-ATPase or 5'-nucleotidase in the same preparations. Inhibition by the E. coli LPS appeared to be noncompetitive in nature, and the calculated Ki was 45 microgram/ml. Since the Na+, K+-ATPase may be responsible for the elaboration of BSIF, inhibition of this enzyme could be the underlying mechanism for the endotoxin-induced cholestasis.

Adenosine Triphosphatases↗

PubMed1977

Some effects of prostaglandins E1 and E2 and of endotoxin injected into the hypothalamus of young chicks: dissociation between endotoxin fever and the effects of prostaglandins.

Prostaglandins E1 and E2 elevated body temperature of young chicks when injected into the hypothalamus at thermoneutrality (31 degrees C). In contrast, they lowered body temperature when so injected below thermoneutrality (16degreesC): the relation of the fall in body temperature to increased heat loss and decreased heat production was examined. 2 The above effects below thermoneutrality were potentiated by pretreatment with inhibitors of prostaglandin synthetase and possible reasons for this potentation are given. 3 The O-somatic antigen of Shigella dysenteriae consistently evoked hyperthermia when injected into the hypothalamus, irrespective of whether the chicks were within or below thermoneutrality. 4 Pretreatment with prostaglandin synthetase inhibitors failed to prevent the onset of endotoxin fever; however, duration of the fever, induced by intrahypothalamic injection of the O-somatic antigen of Shigella dysenteriae was reduced. 5 The intrahypothalamic injection, belwo thermoneutrality of prostaglandins E1, E2, noradrenaline, 5-hydroxytryptamine or carbachol reversed endotoxin fever, inducing even substantial falls in body temperature. 6 While the results cast some doubts on the role of prostaglandins of the E series as mediators of endotoxin fever in chicks, they cannot be eliminated as mediators until the significance of the reduction in duration of the pyrexic response by indomethacin and 5,8,11,14-eicosatetraynoic acid, and the degree of synthesis inhibition attained, are known.

5,8,11,14-Eicosatetraynoic Acid↗

PubMed1979

Polymyxin B sulfate modification of bacterial endotoxin: effects on the development of endotoxin shock in dogs.

The effects of endotoxin (lipopolysaccharide [LPS]) on the pathogenesis of canine endotoxin shock were compared with those of LPS which had interacted with polymyxin B sulfate prior to administration. Both LPS and polymyxin B-modified LPS caused comparable early decreases in aortic blood pressure, leukocyte and platelet numbers, and serum complement levels. However, in dogs receiving polymyxin B-modified LPS the late hypotensive phase was significantly ameliorated and lethality was significantly decreased. These data indicate that polymyxin B-modified LPS, though significantly less lethal than unmodified LPS, was capable of major interactions with several components of the humoral defense system, and support the concept that such interactions are not determinative in the pathogenesis of canine endotoxin shock.

Animals↗

PubMed1978

[Study of the structure and function of endotoxins with the aid of enzymes. 2. Modification of Salmonella paratyphi B endotoxin with lysozyme and lipase].

Endotoxin preparations from the S. paratyphi B cultures, isolated by various methods, were treated with lysozyme (splitting of beta-1,4-glycoside links of lipid A) and lipase of the pancreas (splitting of complex ester links of glycerophosphatides). Lysozyme and, to a lesser extent, lipase, were capable of partial depression of the toxic endotoxin function. The process of enzymatic detoxication coursed selectively, without influencing the serological and immunological activity of the preparations. Suppositions are put forward on the complicated nature of the toxic endotoxin function manifestation and possibility of provision of detoxication effect by specific actions differing by the point of application.

Antitoxins↗

PubMed1976

Bone marrow reactions to E. coli endotoxin or Pseudomonas original endotoxin protein in germ-free mice.

Comparative studies between germ-free and conventional mice were made as to the bone marrow reactions to E. coli endotoxin and Pseudomonas aeruginosa OEP. With the direct smear method of the bone marrow reactions, it was found that conventional mice were more vulnerable than germ-free mice. Conventional mice were more sensitive also as to lethality. With the absolute count method of the bone marrow reactions, conventional mice were more vulnerable than germ-free mice on the increase of red blood cell number in the marrow which reflected damage of the circulation, whereas germ-free mice were more sensitive than conventional mice as to the decrease of nucleated cell number in the marrow which resulted from leukopenia and leukocytosis in the peripheral circulation. This finding as to the nucleated cell number was more remarkable in mice given OEP than in the mice given endotoxin.

Animals↗

PubMed1978