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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↗
PubMed1966

Effects of bacterial endotoxin on rabbit platelets. IV. The divalent ion requirements of endotoxin-induced and immunologically induced platelet injury.

The divalent ion requirements of rabbit platelet injury by endotoxin have been defined by the use of various anticoagulant solutions and have been compared to the divalent ion requirements of platelet injury produced by addition of antigen to immune platelet-rich plasma. The endotoxin-platelet interaction takes place in citrated blood. Platelet damage by antigen is inhibited by citrate, but preincubation of antigen and immune platelet-poor plasma in the absence of citrate results in a substance, presumably antigen-antibody complement complex, which then does injure platelets in the presence of citrate. Neither endotoxin nor preincubated antigen injures platelets in the presence of sodium EDTA in concentrations sufficient to interact with all divalent cations present in plasma. These observations have been interpreted by viewing the platelet-endotoxin interaction as a consequence of platelet phagocytosis of endotoxin, a reaction not requiring complement but requiring definite small concentrations of divalent cations. The interaction of antigen and platelets is regarded as a two phase reaction, the first requiring the participation of complement and concentrations of divalent cation larger than those provided in citrated plasma, the second requiring smaller concentrations of divalent cation, no further participation of complement, and active in citrated plasma. This second phase is regarded as representing platelet phagocytosis of immune complexes.

Animals↗
PubMed1995

Application of a new perchloric acid treatment method to measure endotoxin by an endotoxin-specific chromogenic Limulus test in neonatal septicemia.

The endotoxin in blood was measured to establish both the cut-off value and to detect Gram-negative septicemia. We employed a new perchloric acid treatment method using an endotoxin-specific chromogenic Limulus test (Endospecy test). The cut-off value of endotoxin in blood was 11.2 pg/mL. All cases of septicemia (n = 7) showed high values of endotoxin. Three cases were Group B streptococci, and two cases were Escherichia coli. The others were showed to be negative in blood cultures. The paired values of endotoxin titers during a 48 h interval were useful to evaluate the effectiveness of antibiotics.

Bacteremia↗
PubMed1987

Effects of endotoxins from Bacteroides intermedius and Escherichia coli on cytotoxic and lysosomal activity in peritoneal macrophages from endotoxin responder and low responder mouse strains.

Peritoneal macrophages from normal mice strains (C3H/Tif and C57BL/6J) and from the endotoxin (lipopolysaccharide, LPS) low responder strain (C3H/Hej were exposed to two structurally different endotoxins from Bacteroides intermedius and Escherichia coli in vitro. Intracellular activity of a lysosomal enzyme (acid phosphatase) and macrophage mediated cytotoxic activity against a tumor cell line (L929) were tested. Both endotoxins caused increased levels of acid phosphatase activity in normal mice macrophages. No change was obtained in the C3H/Hej macrophages exposed to E. coli LPS; however, the B. intermedius LPS was able to strongly elevate intracellular enzyme level in the C3H/Hej low responder macrophages. Cytotoxic activities were investigated in macrophage supernatants and in co-cultures of stimulated macrophages and target cells. Cytotoxic activity evaluated by measuring release of radioactivity from 14C-thymidine labelled tumor cells was increased with both endotoxins in normal mouse macrophages, but not in non-responder macrophages. When macrophage-mediated effects on tumor cells were tested by counting target cells left per culture, a reduction in target cell number was observed in endotoxin-treated low responder macrophage as well as in normal strain macrophage cultures more pronounced, however, in the normal strain. Cell contact between cytotoxic macrophages and target cells was verified by scanning electron microscopy. The results suggest that LPS effects on macrophages are dependent upon the functional parameters studied, and that the chemical composition of a particular LPS is important for its selective effects on macrophage functions.

Animals↗
PubMed2004

Endotoxin-mediated disturbance of hepatic cytochrome P450 function and development of endotoxin tolerance in the rat model of dextran sulfate sodium-induced experimental colitis.

Hepatobiliary abnormalities have been described in patients with chronic inflammatory bowel diseases. Hepatic cytochrome P450 (P450)-dependent drug-metabolizing enzyme activities and susceptibility to a hepatotoxin, d-galactosamine, were determined in rats with dextran sulfate sodium (DSS)-induced colitis to assess whether liver function is affected in the model of inflammatory bowel disease. Colitis was induced by treatment of rats with 3% DSS in drinking water for 7 days. Liver microsomes for enzyme activities and serum for biological analysis were prepared from the rats with colitis, along with untreated and lipopolysaccharide (LPS)-treated rats. Other rats received intraperitoneal injection of d-galactosamine to assess their susceptibility to the toxin-induced liver injury. Treatment of rats with DSS resulted in not only colitis but also decreases in hepatic P450-dependent drug-metabolizing enzyme activities. Elevated endotoxin was found in portal blood, which was not associated with liver injury. The potency and the isoform selectivity in the suppression of the P450 enzymes by DSS treatment were similar to those of LPS-treated rats. Coadministration of antibiotics, polymyxin B or metronidazole, with DSS protected rats from decreases in some but not all P450 enzyme activities, indicating partial involvement of bacterial endotoxin in the P450 decreases. The rats with colitis were less susceptible than untreated rats to d-galactosamine-induced liver injury and TNF-alpha production, suggesting development of endotoxin tolerance in DSS-colitis. In conclusion, these results suggest that the DSS-colitis leads to endotoxin-mediated down-regulation of hepatic P450 enzymes and protection against d-galactosamine-induced liver injury, probably due to endotoxin tolerance.

Administration, Oral↗
PubMed1994

Production of multiple delta-endotoxins by Bacillus thuringiensis: delta-endotoxins produced by strains of the subspecies galleriae and wuhanensis.

A method was developed to assess the number of delta-endotoxins contained in Bacillus thuringiensis entomocidal crystals. It utilized proteolytic conversion of 130-kDa protoxin into 60- to 65-kDa "true" toxin via limited proteolysis with trypsin and separation of stable N-terminal domains by fast-performance liquid chromatography. Immunodiffusion experiments and N-terminal sequence determination (applied to the major component isolated by SDS-PAGE) completed the analysis of the crystal protein composition. The application of this approach to crystals produced by cells of B. thuringiensis subsp. galleriae and wuhanensis allowed us to identify at least seven and eight different delta-endotoxins, respectively. Among those delta-endotoxins assigned to previously described families, CryIA, CryID, CryIF, and CryIG were found, as well as crystal proteins, which possess N-terminal amino acid sequences very different from those of all known delta-endotoxins. Possible functional consequences of delta-endotoxin multiplicity are discussed.

Amino Acid Sequence↗
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↗
PubMed1989

Endotoxins and anti-endotoxins (their relevance to the anaesthetist and the intensive care specialist).

Endotoxins (lipopolysaccharides, LPS) are potent bacterial poisons always present within the intestines in considerable amounts. Several pathophysiological conditions such as hypovolaemia, hypoxia, intestinal ischaemia, burns and radiation lead to a breakdown in the barrier and depending upon the extent of the injury, endotoxins enter the systemic circulation in increasing amounts. Antibiotics do not inactivate the endotoxins which continue to exert their toxic effects leading to nausea, vomiting, diarrhoea, fever, disseminated intravascular coagulation, vascular collapse and organ failure. When nonabsorbable antibiotics are given prior to the insult, systemic endotoxaemia is prevented. Immunotherapy, using anti-lipopolysaccharide IgG, inactivates plasma endotoxins, destroys gram-negative bacteria and opsonises them and may become a major form of therapy. An outline of endotoxin and anti-lipopolysaccharide and its importance to the anaesthetist and intensive care specialist is presented.

Animals↗
PubMed1980

Endotoxin enhanced adjuvant effect of liposomes, particularly when antigen and endotoxin are incorporated within the same liposome.

Endotoxin has been shown to enhance the adjuvant effect of liposomes to protein antigens. When a weak antigen and endotoxin were associated with the same liposomes, antibody production could be detected 3 days (72 hours) after injection of the antigen-liposome-endotoxin preparation. When antigen and endotoxin were associated with different liposomes and these antigen-liposome and endotoxin-liposome preparations were injected simultaneously, the adjuvant effect of the liposomes was enhanced also, but not enough to detect antibody production on day 3.

Adjuvants, Immunologic↗
PubMed1992

Endotoxin removed from hemoglobin solution using polymyxin-B immobilized fibre (PMX-F) followed by a new turbidometric endotoxin assay.

Endotoxin contamination in modified hemoglobin can result in side effects. Accurate measurement and effective elimination of endotoxin are important in producing safe hemoglobin preparation. A new turbidometric endotoxin assay (Toxinometer) was studied, in which absorbance of wavelength was applied at 660 nm. This method is not affected by the presence of hemoglobin in solution. This way, toxinometer can accurately measure endotoxin concentration in hemoglobin solution. For the elimination of endotoxin, polymyxin-B immobilized fiber (PMX-F) was studied in-vitro and compared with commercial materials. The PMX-F was found to be a convenient and less expensive approach.

Animals↗
PubMed2000

[The Endotoxin 10,000 Reference Standard of the National Institute of Health Sciences (the Japanese Pharmacopoeia Endotoxin 10,000 Reference Standard) (Control 0001)].

To establish the fourth lot (Control 0001) of the Endotoxin 10,000 Reference Standard of the National Institute of Health Sciences (the Japanese Pharmacopoeia Endotoxin 10,000 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 20,000 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 fourth lot of the Endotoxin 10,000 Reference Standard containing 20,000 EU per vial.

Endotoxins↗
PubMed2002

[The Endotoxin 10000 Reference Standard of the National Institute of Health Sciences (the Japanese Pharmacopoeia Endotoxin 10000 Reference Standard) (Control 0211)].

To establish the fifth lot (Control 0211) of the Endotoxin 10000 Reference Standard of the National Institute of Health Sciences (the Japanese Pharmacopoeia Endotoxin 10000 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 a s containing approximately 16,000 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 fifth lot of the Endotoxin 10000 Reference Standard containing 16,000 EU per vial.

Endotoxins↗
PubMed1983

Cellular effects of endotoxin in vitro. I. Effect of endotoxin on mitochondrial substrate metabolism and intracellular calcium.

Intramitochondrial substrate metabolism was examined in cultured neuroblastoma NB41A3 cells exposed to endotoxin in order to elucidate possible causes for the changes in [ATP]/[ADP][Pi] and [NAD+]/[NADH] reported by us previously in these cells [1]. Flux through pyruvate dehydrogenase (PDH), measured with [1-14C]-pyruvate, was inhibited by 54% within 10 min in endotoxin-treated cells (0.99 nmol/min/mg dry wt vs 0.46 nmol/min/mg dry wt). In contrast, flux through 2-oxoglutarate dehydrogenase, measured with [1-14C]-glutamate was unaltered (0.79 nmol/min/mg dry wt). Dichloroacetate, an inhibitor of PDH kinase, restored flux through PDH to control levels. In endotoxin-treated cells, only 44% of the total PDH complex was in the active (nonphosphorylated) form as compared to 72% in control cells. Equilibrium uptake studies with 45Ca2+ and atomic absorption measurements showed that intracellular [Ca2+] in endotoxin-treated cells was about 20% lower than in control cells. It is postulated that binding of endotoxin to the plasma membrane triggers a sequence of events that lead to an initial decline in intracellular calcium concentration and that this latter event may be responsible for the inhibition of PDH phosphatase and consequent conversion of the complex to its inactive phosphorylated form.

Animals↗
PubMed1983

Stimulation of human peripheral lymphocytes with endotoxin and radiodetoxified endotoxin.

The effects of parent endotoxin and radiodetoxified endotoxin on human peripheral lymphocytes were compared in experiments in vitro. Radiodetoxified endotoxin is able to exceed the degree of the stimulation induced by parent endotoxin and its stimulatory effect. At the same time, no change was observed in the presence of autologous serum. Radiodetoxified endotoxin did not inhibit the phytohaemagglutinin-induced proliferative response.

Cells, Cultured↗
PubMed1983

Granulocyte activation by endotoxin. I. Correlation between adherence and other granulocyte functions, and role of endotoxin structure on biologic activity.

Reminiscent of high concentrations of formylated chemotactic peptides, another group of bacteria-derived products, the lipopolysaccharides and lipid A, stimulate PMN adherence to petri dishes. Attachment and spreading of PMN is accompanied by intense release of secondary granule constituents and marked stimulation of the hexose monophosphate shunt activity. Dose-response studies with endotoxin preparations of diverse activity show that induction of PMN adherence, enzyme release, and respiratory burst activation are highly correlated, suggesting that this functional triad is mediated by a common mechanism. Hyperadhesiveness inducing concentrations of the chemotactically inert endotoxin lead to marked inhibition of PMN migration without affecting the direction-finding mechanism of the cell toward formylated peptides and C-derived chemotaxin(s). Endotoxin preparations at a lower grade of aggregation are more active, and the polysaccharide chains of the molecule are not essential with respect to PMN stimulation. Under our experimental conditions, endotoxin-induced stimulation of PMN is not inhibited by indomethacin, suggesting independence of cyclooxygenase-derived products. This type of PMN activation may play an important role in endotoxin-mediated tissue damage in vivo. Furthermore, hyperadhesion-induced inhibition of PMN migration to inflammatory sites during endotoxemia might hamper host resistance.

Arachidonic Acids↗
PubMed1999

Endotoxin tolerance in rats: expression of TNF-alpha, IL-6, IL-10, VCAM-1 AND HSP 70 in lung and liver during endotoxin shock.

Endotoxin can induce a state of tolerance against its own pathological effects, commonly referred to as endotoxin tolerance. This phenomenon has been found to be associated with reduced serum levels of cytokines such as TNF-alpha, IL-1, IL-6 and IL-10. In the present study the expression of TNF-alpha, IL-6, IL-10, the adhesion molecule VCAM-1 and the heat shock protein 70 was determined in vivo in lung and liver of LPS-tolerant and naive rats by means of semiquantitative RT-PCR after i.v. LPS injection. TNFalpha, IL-6, IL-10, HSP 70 and VCAM-1 were induced in lung and liver after LPS injection. In liver and lung of endotoxin-tolerant rats TNF-alpha and IL-6 were induced to a lower degree after LPS treatment when compared to non-tolerant controls. The LPS-induced IL-10 expression was also slightly attenuated in the lung of tolerant rats, but in the liver no differences between tolerant and non-tolerant animals were observed. HSP 70 and VCAM-1 were expressed after systemic LPS treatment in liver and lung. The degree of induction, however, was the same in tolerant and untreated controls. The presented data show that endotoxin tolerance is reflected by a reduced cytokine expression in lung and liver in vivo. On the other hand, levels of expression of the adhesion molecule VCAM-1 and the stress protein HSP 70 do not appear to be changed by endotoxin tolerance.

Animals↗
PubMed1999

IL-18-deficient mice are resistant to endotoxin-induced liver injury but highly susceptible to endotoxin shock.

IL-18 is an IL-1-related cytokine which shares biological functions with IL-12. These include the activation of NK cells, induction of IFN-gamma production and Th1 cell differentiation. In this study we analyzed the effect of IL-18 deficiency on lipopolysaccharide (LPS)-induced liver injury and endotoxin shock in Propionibacterium acnes-primed mice. P. acnes-primed IL-18-deficient (IL-18KO) mice showed resistance to LPS-induced liver injury. Unexpectedly, P. acnes-primed IL-18KO mice were highly susceptible to LPS-induced endotoxin shock. Serum level of tumor necrosis factor (TNF)-alpha were markedly elevated (approximately 10-fold higher) within 1.5 h after LPS challenge in IL-18KO mice as compared with wild-type mice. Anti-TNF-alpha antibody administration to IL-18KO mice was significantly protective against endotoxin-induced lethality. P. acnes-primed IL-18KO macrophages produced approximately 6-fold more TNF-alpha protein than did P. acnes-primed wild-type control macrophages. Taken together, these findings demonstrate that IL-18 is responsible for the progression of endotoxin-induced liver injury as well as down-regulation of endotoxin-induced TNF-alpha production in P. acnes-primed mice.

Animals↗
PubMed1964

EFFECTS OF BACTERIAL ENDOTOXIN ON RABBIT PLATELETS. 3. COMPARISON OF PLATELET INJURY INDUCED BY THROMBIN AND BY ENDOTOXIN.

The platelet injury produced by bacterial endotoxin and thrombin have been compared in studies utilizing citrated rabbit platelet-rich plasma. Endotoxin-induced platelet injury is characterized by a lag period, is progressive, and does not produce gross clot formation. Thrombin-induced platelet injury is immediate, non-progressive, and is associated with clot formation. The quantity of thrombin required to produce clot formation in this citrated system is less than that required to produce release of platelet 5-hydroxytryptamine. The endotoxin-induced platelet injury required extremely large quantities of heparin for inhibition. The platelet injury induced by thrombin can be inhibited by small quantities of heparin. It is concluded that the injurious effects of endotoxin on platelets is mediated through some mechanism other than thrombin formation.

Animals↗