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PubMed2000

[The role of bacterial endotoxins, receptors and cytokines in the pathogenesis of septic (endotoxin) shock].

Sepsis, resistant to therapy, results in the development of septic (endotoxin) shock. The latter is caused by the endotoxins of different Gram-negative bacteria. Endotoxin (bacterial lipopdisacharide--LPS) interacts with cells through specific membrane or plasma soluble endotoxin receptors (sCD14, mlD14, LBP, CD13/CD14, CD16, CD116/CD18, L-selectin, etc.). Endotoxin interaction with the mCD14 receptor of the monocytes, macrophages and the neutrophils results in the production of a number of proinflammatory cytokines--tumor necrosis factor alpha (TNF alpha), interleukines 1 and 6 (IL-1 and IL-6, etc), antiinflammatory cytokines--interleukines 10 and 12 (IL-10 and IL-12), cell adhesion molecules (P-selectin, E-selectin, ICAM-1, VCAM-1, etc.) and inducible enzymes: inducible NO synthase (iNOS), inducible phospholipase A2 (cPL-A2), inducible cyclooxygenase (COX-2). All pathologic processes in the structure and function of human body during endotoxin shock are a result of the disbalance of a number of mediators with a proinflammatory and antiinflammatory effects.

Cell Adhesion Molecules↗

PubMed2001

[The Endotoxin 100 Reference Standard of the National Institute of Health Sciences (the Japanese Pharmacopoeia Endotoxin 100 Reference Standard) (Control 0101)].

To establish the second lot (Control 0101) of the Endotoxin 100 Reference Standard of the National Institute of Health Sciences (the Japanese Pharmacopoeia Endotoxin 100 Reference Standard), a candidate standard (CS) was prepared and then evaluated. The potency of the CS was assayed against USP Endotoxin Reference Standard (Lot G-1) and defined as containing approximately 100 endotoxin units (EU) per vial by a collaborative study in which 5 laboratories participated. Based on the results, the CS was authorized to be the second lot of the Endotoxin 100 Reference Standard containing 100 EU of endotoxin per vial.

Endotoxins↗

PubMed2002

[The Endotoxin 100 Reference Standard of the National Institute of Health Sciences (the Japanese Pharmacopoeia Endotoxin 100 Reference Standard) (Control 0201)].

To establish the third lot (Control 0201) of the Endotoxin 100 Reference Standard of the National Institute of Health Sciences (the Japanese Pharmacopoeia Endotoxin 100 Reference Standard), a candidate standard (CS) was prepared and then evaluated. The potency of the CS was assayed against USP Endotoxin Reference Standard (Lot G-1) and defined as containing approximately 130 endotoxin units (EU) per vial by a collaborative study in which 5 laboratories participated. Based on the results, the CS was authorized to be the third lot of the Endotoxin 100 Reference Standard containing 130 EU of endotoxin per vial.

Endotoxins↗

PubMed1987

Quantitative measurement of endotoxin in canine plasma using the new endotoxin-specific chromogenic test.

Endospecy (a lyophilized mixture of factor G-free limulus coagulation enzymes and chromogenic substrate, Boc-Leu-Gly-Arg-pNA) coupled with modified perchloric acid (PCA) pretreatment was carried out for the quantitative measurement of endotoxin in canine plasma. The endotoxin recovery from normal canine plasma was 99.9 +/- 7.7% (n = 20). The full recovery of endotoxin illustrated the applicability of the modified PCA pretreatment to the Endospecy in removal of interfering factors in a canine plasma. The normal canine plasma endotoxin level was less than 3.0 pg.ml-1 when Escherichia coli 0111:B4 endotoxin was used as a reference. The canine plasma endotoxin levels were markedly high(1-40 ng.ml-1) at 5 min after intravenous administration of 25 micrograms.Kg-1 (total 150-200 micrograms).

Animals↗

PubMed1987

A comparison of Escherichia coli endotoxin single bolus injection with low-dose endotoxin infusion on pulmonary and systemic vascular changes.

The purpose of this study was to compare effects of single bolus endotoxin injection with sustained low-dose endotoxin infusion on systemic and pulmonary hemodynamics in anesthetized dogs. When administered as a bolus (.01 mg/kg), endotoxin induced systemic vascular changes whose evolution could be divided into two consecutive phases. In the early phase, marked hepatic venoconstriction caused a rise in portal pressure followed by abrupt decreases in both cardiac output and blood pressure. Mean pulmonary artery pressure remained unchanged. Because of lowered blood flow, both peripheral and pulmonary resistances increased. The rise in the latter was due to a prominent vasoconstriction of pulmonary arteries. Following a partial spontaneous recovery from shock, the late phase was characterized by a low-output state combined with high systemic vascular resistances. In contrast, when endotoxin was given at a slow infusion rate (250 ng/kg/min) over a 2-hour period of time, cardiovascular effects were basically different from the preceding ones, and they were measurable only after a certain period of time had elapsed from the start of endotoxin insult. First, blood pressure decreased gradually, while cardiac output remained almost unchanged. Therefore, peripheral resistance was decreased. Second, in the pulmonary circulation, the site of vasoconstriction was shifted from arteries to veins. We conclude that there is a fundamental difference in the response of the dog's systemic and pulmonary circulation as a function of endotoxin administration as either a bolus or slow infusion. This difference might be due to sudden elevated portal pressure responsible for an abrupt cardiovascular collapse in dogs subjected to bolus injection.

Animals↗

PubMed1982

Plasma zinc and iron concentrations as measurements for evaluating the influence of endotoxin-neutralizing agents in Escherichia coli endotoxin-induced mastitis.

The influence of bacterial lipopolysaccharides on plasma Zn and Fe concentrations and the endotoxin-neutralizing capacity of polymyxin B was studied in 3 dairy cows. Also, the feasibility of using plasma Zn and Fe concentrations as measurements for evaluating the influence of endotoxin-neutralizing agents in Escherichia coli endotoxin-induced mastitis was studied. A positive relationship was ascertained between the dose of endotoxin given intramammarily (IMM) and the effect on mean values of plasma Zn and Fe concentrations. Seemingly, IMM administration of polymyxin B-sulfate before the IMM administration of E coli endotoxin partially blocked the effects of endotoxin, as shown by decreases in plasma Zn and Fe.

Animals↗

PubMed1981

[Effect of pretreatment with radiation-detoxified endotoxin on endotoxin shock in dogs].

The protective action of the radiation detoxified endotoxin preparation (Tolerin) on the endotoxin shock of dogs was studied. Endotoxin shock was induced by the intravenous administration of 2 mg/kg of Escherichia coli endotoxin. It was found that the intraperitoneal administration of 4 mg of radiation-detoxified endotoxin (Tolerin) 48 hours prior to the inducement of shock prevents the drop in blood pressure and the decrease of cardiac output which promptly appear in the acute phase of endotoxin shock.

Animals↗

PubMed1995

Inhibition of endotoxin-induced activation of the coagulation and fibrinolytic pathways using a recombinant endotoxin-binding protein (rBPI23).

A recombinant endotoxin-neutralizing protein, rBPI23, was shown to partially prevent endotoxin-induced activation of the fibrinolytic and coagulation systems in experimental endotoxemia in humans. In a placebo-controlled, blinded crossover study, eight volunteers were challenged twice with an intravenous bolus injection of endotoxin (40 EU/kg of body weight) and concurrently received either rBPI23 (1 mg/kg) or placebo (human serum albumin, 0.2 mg/kg). rBPI23 treatment significantly lowered the endotoxin-induced fibrinolytic response, ie, reduced the release of tissue-type plasminogen activator, urokinase-type plasminogen activator, plasminogen activator inhibitor antigen, and complex formation of plasmin alpha 2-antiplasmin (P = .0078 for each). Plasminogen activator inhibitor activity was also reduced, but not significantly according to the Hochberg method (P = .0304). The endotoxin-induced activation of the procoagulant state as reflected by increase in F1 + 2 fragments and TAT complexes was blunted by rBPI23 infusion (P = .0391 [not significant according to the Hochberg method] and .0078, respectively). These results indicate that rBPI23 is capable of reducing both the activation of the fibrinolytic and the coagulation systems after low-dose endotoxin infusion in humans.

Anticoagulants↗

PubMed1995

Recombinant endotoxin-binding protein (rBPI23) attenuates endotoxin-induced circulatory changes in humans.

In the present study the protective effect of a recombinant endotoxin-binding protein rBPI23 on the circulatory changes in experimental endotoxemia in humans was investigated. In a controlled, blinded crossover study, eight volunteers were challenged twice with an intravenous bolus injection of endotoxin (40 EU/kg body weight), and concurrently received either rBPI23 (1 mg/kg) or placebo (human serum albumin, 0.2 mg/kg). Hemodynamic parameters were obtained non-invasively by means of M-mode, two-dimensional, and Doppler echocardiography. rBPI23 significantly reduced indices of the endotoxin-induced hyperdynamic circulation. rBPI23 treatment significantly reduced increase in cardiac index (P = 0.0156). rBPI23 treatment diminished the endotoxin-induced decrease in systemic vascular resistance index (P = 0.0304). rBPI23 did not prevent the endotoxin-induced rise in body temperature and systolic, diastolic and mean arterial pressure were not significantly different in the rBPI23- and placebo-treatment arm. Both treatment periods showed a small reduction in end diastolic and end systolic volumes. rBPI23 treatment slightly reduced the increase in M-mode ejection fraction and fractional shortening. These results indicate that rBPI23 is capable of attenuating the potentially deleterious circulatory effects of endotoxin in humans.

Adult↗

PubMed1998

Endotoxin-neutralizing protein protects against endotoxin-induced endothelial barrier dysfunction.

Bacterial lipopolysaccharide induces tyrosine phosphorylation of paxillin, actin reorganization, and opening of the transendothelial paracellular pathway through which macromoles flux. In this study, lipid A was shown to be the bioactive portion of the lipopolysaccharide molecule responsible for changes in endothelial barrier function. We then studied whether endotoxin-neutralizing protein, a recombinant peptide that is derived from Limulus antilipopolysaccharide factor and targets lipid A, could block the effects of lipopolysaccharide on protein tyrosine phosphorylation, actin organization, and movement of 14C-bovine serum albumin across bovine pulmonary artery endothelial cell monolayers. In the presence of serum, a 6-h exposure to lipopolysaccharide (10 ng/ml) increased transendothelial 14C-albumin flux compared to the simultaneous media control. Coadministration of endotoxin-neutralizing protein (> or =10 ng/ml) with lipopolysaccharide (10 ng/ml) protected against lipopolysaccharide-induced barrier dysfunction. This protection was dose dependent, conferring total protection at endotoxin-neutralizing protein/lipopolysaccharide ratios of > or =10:1. Similarly, endotoxin-neutralizing protein was capable of blocking the lipopolysaccharide-induced endothelial cell responses that are prerequisite to barrier dysfunction, including tyrosine phosphorylation of paxillin and actin depolymerization. Finally, endotoxin-neutralizing protein cross-protected against lipopolysaccharide derived from diverse gram-negative bacteria. Thus, endotoxin-neutralizing protein offers a novel therapeutic intervention for the vascular endothelial dysfunction of gram-negative sepsis and its attendant endotoxemia.

Actins↗

PubMed2006

Low dose endotoxin priming is accountable for coagulation abnormalities and organ damage observed in the Shwartzman reaction. A comparison between a single-dose endotoxemia model and a double-hit endotoxin-induced Shwartzman reaction.

The clinical response of sepsis to a systemic inflammatory infection may be complicated by disseminated intravascular coagulation or DIC. In order to experimentally study the syndrome of DIC, we aimed for a severe sepsis model complicated by disseminated coagulation. Most-simplified-experimental models describing coagulation abnormalities as a consequence of sepsis are based on single dose endotoxemia. The so called-Shwartzman reaction contrarily, is elicited by a low dose endotoxin priming followed by an LPS challenge and is characterized by pathological manifestations that represent the syndrome of DIC. In order to investigate whether the Shwartzman reaction is superior to a single endotoxin challenge as a model for sepsis-induced DIC and to determine what the pathological effect is of an encounter of low endotoxin prior to an LPS challenge, we undertook the present study. In this study we demonstrate that low-dose endotoxin priming prior to an LPS challenge in the Shwartzman reaction is accountable for micro-vascular thrombosis in lung and liver and subsequent (multi-) organ failure, not observed after a single-dose endotoxin challenge, which indicates that the Shwartzman reaction is well suited-model to study sepsis-induced DIC adversities. Remarkably, only minor differences in the innate immune response were established between the single-dose endotoxin challenge and the Shwartzman reaction.

Journal Article↗

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↗

PubMed1984

Haemorrhagic tumour necrosis following endotoxin administration. I. Communication: morphological investigation on endotoxin-induced necrosis of the methylcholanthrene (Meth A) tumour in the mouse.

Endotoxin induced necrosis of the Meth A mouse tumour has been investigated using macroscopic, histological and ultrastructural examination methods. On the 8th day after tumour cell transplantation, the animals received a relatively non-toxic dose of the Salmonella abortus equi endotoxin intravenously. The natural history of the tumour necrosis took the following course: The earliest morphological changes could be seen with the electron microscope 90 min after administration of the endotoxin, and were seen as an interstitial oedema with separation of the tumour cells. Haemorrhagic necrosis of the tumour was complete 4 hours after injection, and could be easily recognized with the naked eye. Rejection of the necrotic malignant tumour was complete two weeks after LPS administration. Only minor residual scarring of the belly-wall remained. Haemorrhagic tumour necrosis due to endotoxin can be compared with the localized Shwartzman reaction and probably involves tumour necrotizing factor (TNF). For complete destruction of a tumour by haemorrhagic necrosis the size of the tumour is critical. Certain regression after endotoxin administration depends upon additional T-cell-mediated immunity (provided the tumour is immunogenic). In contrast to the haemorrhagic necrosis, BCG-induced tumour regression is accompanied by granulomatous inflammation, which may be responsible for destruction of the tumour.

Animals↗

PubMed1987

Liver glycogen metabolism in endotoxin shock. II. Endotoxin administration increases glycogen phosphorylase activities in dog livers.

The effects of E. coli endotoxin administration on hepatic glycogen phosphorylase activities in dogs were investigated. Hepatic glycogen phosphorylase activities in both control and endotoxic dogs were inactivated spontaneously by preincubation of enzyme preparations at 25 degrees C. Total glycogen phosphorylase activity was not significantly altered during preincubation. The activity of glycogen phosphorylase a was increased by 83 and 80% at 1 and 2 hr postendotoxin, respectively, without preincubation; and by 203 and 133% at 1 and 2 hr postendotoxin, respectively, after 30 min preincubation. Without preincubation, the glycogen phosphorylase percentage a activity was increased from the control value of 37 to 58% at 1 hr postendotoxin and to 53% at 2 hr postendotoxin. After 30 min preincubation, the glycogen phosphorylase percentage a activity was increased from the control value of 10 to 28% at 1 hr postendotoxin and to 20% at 2 hr postendotoxin. The time required for half maximum inactivation of percentage a activity was 16.5, 33, and 24 min for control, 1 and 2 hr postendotoxin, respectively. Although the Vmax and Km for glucose-1-P for total glycogen phosphorylase were not affected by endotoxin administration, the Vmax for glucose-1-P for glycogen phosphorylase a was increased by 57.3 and 42.7% at 1 and 2 hr postendotoxin, respectively, with no change in the Km values. Glucose inhibited glycogen phosphorylase a activity both in control and endotoxin-injected dogs, but the I50 value was increased by 35% in endotoxin-injected (2 hr) dogs. AMP activated glycogen phosphorylase b activity both in control and endotoxin-injected dogs with no change in A0.5 values between the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Monophosphate↗

PubMed2003

Richard Pfeiffer and Alexandre Besredka: creators of the concept of endotoxin and anti-endotoxin.

Richard Pfeiffer, working with Robert Koch in Berlin, intellectually and experimentally conceived the concept of endotoxin as a heat-stable bacterial poison responsible for the pathophysiological consequences of certain infectious diseases. Pfeiffer's definition of endotoxin included the inability to evoke neutralizing antibodies against this bacterial toxin. Alexandre Besredka, Ilya (Elie) Metchnikoff's successor at the Institut Pasteur in Paris, was the first to demonstrate that, in fact, antibodies could be engendered which were capable of suppressing the poisonous effects of endotoxin. Endotoxin and anti-endotoxin antibodies have since then fascinated researchers of many disciplines and continue to do so, particularly in the fields of diagnosis, prevention, and therapy of severe Gram-negative infections.

Endotoxins↗

PubMed1998

Chromatographic removal of endotoxin from hemoglobin preparations. Effects of solution conditions on endotoxin removal efficiency and protein recovery.

In this work, affinity chromatography was used to remove endotoxin from human hemoglobin preparations with a Sterogene Acticlean Etox column. The effects of solution conditions on endotoxin removal efficiency and protein recovery have been investigated. It has been found that cations Na(+) or Ca(2+) reduced endotoxin removal efficiency from 73% (sample prepared with endotoxin-free water) to 31% (sample prepared with 0.15 M NaCl, ionic strength, I = 0.15 M), and from 73% sample prepared with endotoxin-free water) to 9% (sample prepared with 0.05 M CaCl2, ionic strength, I = 0.15 M). It has also been found that the protein recovery was increased from 90% to 99%, respectively.

Calcium Chloride↗

PubMed1957

The relationship between the vascular manifestations of shock produced by endotoxin, trauma, and hemorrhage. I. Certain similarities between the reactions in normal and endotoxin-tolerant rats.

The vascular effects of lethal doses of E. coli endotoxin, as observed in the mesentery of the rat, resemble the reactions of traumatic and hemorrhagic shock in the following respects: a profound inhibition of arteriolar and precapillary reactivity to topical epinephrine occurs after an initial stage of hyperreactivity; the small veins show failure to relax completely following constrictor doses of epinephrine; and the terminal vessels develop an unusual sensitivity to fluctuations in temperature of the fluid irrigating the tissue. Rats in which tolerance to bacterial endotoxin is induced, by repeated doses given daily, become highly resistant to the lethal effects of both drum trauma and hemorrhagic shock. However, rats in which the adaptation to traumatic shock is produced by repeated exposure to drum trauma, do not develop a significant degree of tolerance to lethal doses of endotoxin. The injection of small non-lethal doses of bacterial endotoxin during non-lethal episodes of trauma or hemorrhage, leads to the development of irreversible shock and death. The bearing of these findings on the problem of the relationship between endotoxin and traumatic shock is discussed.

Animals↗

PubMed1959

Inactivation of endotoxin by a humoral component. IV. Alteration in the immunological properties of typhoid endotoxin.

The immunological properties of typhoid endotoxin were investigated after incubating it with serum under conditions in which EDC (endotoxin-detoxifying component) was operative. Brief interaction of endotoxin in vitro with this system in serum (human, rabbit, mouse) abolished its antigenicity for rabbits. Suitable modification of the host permitted separate elicitation of toxic and antigenic responses to typhoid endotoxin. Endotoxin altered by EDC was still capable of precipitating specific antibody; moreover, it did so in a manner which resembled that of the haptenic polysaccharide.

Animals↗