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PubMed1987

The effects of Escherichia coli endotoxin as a trigger for hepatic infection of rabbits with Fusobacterium necrophorum.

To evaluate the effects of endotoxin in hepatic infection with Fusobacterium necrophorum, rabbits were given several combinations of F. necrophorum and Escherichia coli endotoxin. Severe hepatic necrosis with multiplication of F. necrophorum was induced by inoculation of endotoxin via the bile duct and following inoculation of both endotoxin and F. necrophorum. Inoculation with F. necrophorum alone, preceded by inoculation of endotoxin via the bile duct, also induced hepatic necrosis, whereas rabbits which received a single inoculation of endotoxin or F. necrophorum had only slight necrotic lesions. The pathogenetic mechanism of experimental hepatic infection with F. necrophorum is discussed.

Animals↗
PubMed1982

Immunoradiometric assay of lipid A: a test for detecting and quantitating endotoxins of various origins.

The ability to measure circulating endotoxin in various disease states has been hampered by the lack of a specific and quantitative assay. The test most commonly used has been the Limulus gelation assay, which measures an enzymatic effect of endotoxin rather than the substance itself. Based on a solid-phase immunoradiometric assay previously developed to detect the specific lipopolysaccharide from Escherichia coli 026, a similar assay has been developed for the lipid A moiety of endotoxins. The assay uses rabbit antibodies to lipid A which do not react with ketodeoxyoctonate, myristic or beta-hydroxymyristic acids, and detects lipid A obtained from endotoxins of various origins after acid hydrolysis of lipopolysaccharide. Experiments in rats given exogenous endotoxin suggest that this assay can be useful for quantitation of bacterial endotoxins in serum and for studying the pathophysiology of experimental endotoxemia.

Animals↗
PubMed1990

Removal of endotoxin from protein solutions by phase separation using Triton X-114.

Endotoxin contamination of protein solutions was reduced by a phase separation technique using the detergent, Triton X-114. Protein solutions containing endotoxin were treated with Triton X-114 on ice. The solution was then warmed to 37 degrees C, whereupon two phases formed. The Triton X-114 phase, containing the endotoxin, was precipitated by centrifugation. The first cycle of phase separation produced a 1000-fold reduction of endotoxin from contaminated preparations of cytochrome c, catalase and albumin. Complete removal of endotoxin could be achieved by further cycles of phase separation. Each cycle of phase separation resulted in only a 2% loss of protein, and could be completed within 15 min. The small amount of detergent (0.018%) that persisted in protein solution could be removed by gel filtration or absorption. Proteins treated by this procedure retained normal functions. This phase separation technique provides a rapid and gentle method for removing endotoxin from protein solutions.

Catalase↗
PubMed1996

The use of human monocytoid lines as indicators of endotoxin.

We wish to develop an in vitro test system for pyrogenic substances. A major source of pyrogen activity is endotoxin. Here we describe a highly sensitive endotoxin-monitoring system based on cytokine measurement in human cell lines of myelomonocytoid origin. The following measures were taken to develop an endotoxin monitoring system of high sensitivity. (i) Mono Mac 6 (MM6) and THP-1 cells, which both represent advanced stages of myelomonocytic development, were better suited as endotoxin indicators than the more immature U-937 line. (ii) In order to enhance cell surface expression of CD14, a major lipopolysaccharide (LPS) receptor, cells were pretreated for 2 days with calcitriol. (iii) The use of fetal calf serum (FCS) without detectable endotoxin traces was essential for maintaining a high LPS sensitivity. (iv) Selected subclones of either THP-1 or MM6 were significantly more sensitive LPS indicators than bulk cultures from which the clones originated. (v) Based on stimulation indices, a commercial tumor necrosis factor-alpha (TNF-alpha) immunoassay proved to be a more sensitive LPS indicator than other cytokine assays or the expression of procoagulant activity/tissue factor. Thus we were able to eliminate the disadvantage of previous cell line-based systems (i.e., low sensitivity) without loss of reproducibility which is seen when using fresh blood, monocytes or monocyte-derived macrophages. High endotoxin sensitivity is a prerequisite for a test system specifically indicating pyrogen activity, because it permits the testing of substances at higher dilutions, thereby minimizing nonspecific interference.

Calcitriol↗
PubMed1990

Impairment in the phosphorylation of canine cardiac sarcoplasmic reticulum following endotoxin administration.

Effects of endotoxin administration on the phosphorylation and dephosphorylation of phospholamban in canine cardiac sarcoplasmic reticulum (SR) were studied. Results obtained 4 h after endotoxin administration show that the Ca2(+)-calmodulin dependent phosphorylation of phospholamban was reduced by 17-25% (P less than 0.05). Kinetic analysis reveals that the Vmax values for Ca2+, for calmodulin, and for ATP for the Ca2(+)-calmodulin dependent phosphorylation were significantly decreased, while the S0.5 values (for Ca2+ and calmodulin) and the Km (for ATP) and Hill coefficients (for Ca2+ and calmodulin) remained unaffected during endotoxic shock. The cAMP-dependent phosphorylation of phospholamban measured in the presence of the exogenously added catalytic subunit of the cAMP-dependent protein kinase remained unaffected. The basal/endogenous (cAMP- and Ca2(+)-independent) phosphorylation of phospholamban was significantly decreased after endotoxin administration. The half-time for the dephosphorylation of phospholamban prephosphorylated in the presence of Ca2+ and calmodulin was shortened by 58% (P less than 0.01) in endotoxin shock. These data indicate that the phosphorylation of phospholamban was inhibited while the dephosphorylation was stimulated in canine cardiac SR during endotoxin shock. Since the phosphorylation and dephosphorylation of phospholamban in cardiac SR plays an important role in the control of myocardial contractility, these findings may have a pathophysiological significance in contributing to the understanding of myocardial dysfunction in endotoxin shock.

Animals↗
PubMed1993

The effect of endotoxin on the neonatal erythrocyte.

Intestinal ischemia is considered a major factor in the development of necrotizing enterocolitis (NEC). Despite this, the majority of affected infants lack documentation of clinical events associated with obvious gut hypoperfusion. Recent evidence in adults suggests that endotoxin may impair flow in the microcirculation through alterations in erythrocyte deformability. As the gut serves as a semipermeable reservoir of endotoxin in the stressed neonate, such localized activity may result in intestinal ischemia at the microcirculatory level through alterations in the red cell membrane. This study evaluates the role of endotoxin on neonatal erythrocyte membrane viscosity. Paired anticoagulated whole blood specimens were obtained from the umbilical cord of 10 neonates at delivery. Samples were incubated with either 2 micrograms/mL of E coli endotoxin (LPS) or an equal volume of saline (control). Following incubation, erythrocytes were isolated, washed, and incorporated with the fluorescent membrane probe TMA-DPH. Membrane viscosity was assessed by spectroscopic analysis of the fluorescent emissions induced by excitation of the probe at 365 nm. Results were calculated as anisotropy and analyzed for differences by ANOVA. Endotoxin resulted in a significant increase in red cell membrane viscosity as compared to control (LPS 291.2 +/- 5.1 v Control 271.7 +/- 3.3, P < .01). As the effects of endotoxin are known to be primarily the result of white blood cell (WBC) activation, this study was repeated in an additional 10 neonates in whom WBCs were removed prior to endotoxin/saline incubation.(ABSTRACT TRUNCATED AT 250 WORDS)

Endotoxins↗
PubMed1989

The effect of Escherichia coli endotoxin on the adrenergic control of lipolysis in the human adipocyte.

We investigated the effect of Escherichia coli O127:B8 endotoxins on the adrenergic control of lipolysis in the human adipocyte. Adipose tissue was incubated in vitro with isoproterenol to stimulate the beta-1 receptors, clonidine to stimulate the alpha-2 receptors, and theophylline to stimulate the subreceptor mechanism. Using a dual radioisotope technique, a lipolysis factor was calculated for each sample. The basal lipolysis factor was significantly (P less than 0.006) decreased 31% with endotoxin. beta-1 adrenergic receptor stimulation (isoproterenol, 1 X 10(-8) to 1 X 10(-4) M) was significantly decreased an average of 31% with E. coli endotoxin. The beta-1 receptor responsiveness was also significantly (P less than 0.02) decreased but not the receptor sensitivity. This indicated an alteration in the post beta receptor mechanism. The various components of the post beta-1 adrenergic mechanism were stimulated including the beta-1 receptor, the G protein, adenylase cyclase, and the lipase phosphorylase. The results indicated a significant 24.2% reduction of the beta-1 receptor and a 25.4% reduction in G protein stimulation. Thus the E. coli endotoxin effect on the beta adrenergic mechanism is at the G protein. The endotoxin had no effect on the alpha-2 receptor stimulation nor the theophylline stimulation of the subreceptor lipolysis. This study indicates that E. coli endotoxin (O127:B8) decreases in vitro beta adrenergic stimulation of human adipocyte lipolysis, and this effect can be partially reversed by theophylline.

Adipose Tissue↗
PubMed1992

The effect of dexamethasone and endotoxin administration on biliary IgA and bacterial adherence.

Adherence of bacteria to the intestinal epithelial cell may be the crucial initiating event for invasion and translocation and is normally prevented by both immune (IgA) and nonimmune (mucus, peristalsis, desquamation) mucosal defense mechanisms. The purpose of the present study was to examine the effect of endotoxin administration on mucosal immunity and to define the role of glucocorticoids, commonly released during endotoxicosis, in this process. Thirty female Fisher rats were randomly assigned to three groups of 10 animals each. Group I (CONT), was fed rat chow and H2O ad lib., Group II (DEX) was administered 0.8 mg/kg subcutaneously of dexamethasone, and Group III (ETX) was given 1 mg/kg of endotoxin. Twenty-four hours later animals were sacrificed and mesenteric lymph nodes and vigorously washed stool-free ceca were collected and cultured. Bile was collected and assayed for IgA from 5 animals in each group. A significant decrease (P < 0.05) in secretory IgA was noted in animals treated with either dexamethasone or endotoxin (CONT = 332 +/- 42, DEX = 78 +/- 24, ETX = 68 +/- 16 micrograms/mg protein +/- SEM). No difference in S-IgA between animals in the dexamethasone-treated group and the endotoxin-treated group was noted (P = NS). A statistically significant increase (P < 0.001) in bacteria adherent to the cecal wall in both the dexamethasone-treated rats and the endotoxin-treated rats over that in = 7.5 +/- 0.8, CONT = 6.4 +/- 0.6 cfu/g(log10) +/- SD). Our results suggest that endotoxin or glucocorticoid administration results in significant bacterial adherence to the cecal mucosa and a decrease in IgA.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Prevention of the toxicity of erythromycin estolate in the perfused rat liver by endotoxin.

The possibility that endotoxin pretreatment could prevent the hepatotoxic effects of erythromycin estolate (EE) was investigated using the isolated perfused rat liver. The addition of E. coli endotoxin (25 micrograms/ml) to the perfusate, 30 min prior to EE administration at 150 or 200 microM, significantly ameliorated the decreases in bile and perfusate flow caused by either concentrations of the drug in control liver preparations. This phenomenon was also studied using liver isolated from rats pretreated in vivo with endotoxin for three days. In these preparations, EE at both concentrations did not alter bile flow and caused reductions of perfusate flow which were far less than those observed in untreated control livers. Furthermore, in livers from endotoxin-treated rats EE induced less reduction of bile acid excretion and, at 150 microM, it did not increase the bile to perfusate ratio of sucrose seen in control preparations after the drug, which may be an expression of altered hepatocytic membrane permeability. Since it is known that both endotoxin and EE interact with membranes, it is suggested that the "protective" effects of endotoxin may occur at the membrane level.

Animals↗
PubMed1989

Endotoxin-induced reduction of beta-adrenergic binding sites on splenic lymphocytes in vivo and in vitro: its modulation by anterior hypothalamic lesions.

Bacterial endotoxin induced a 38% decrease in the number of beta-adrenergic binding sites (Bmax) on splenic lymphocytes, four days after intraperitoneal administration to guinea pigs. No change in the affinity (Kd) for [125-I]-cyanopindolol ([125-I]-CYP) binding was observed. Incubation of guinea pig splenocytes in vitro with different concentrations of bacterial endotoxin for 24 hours resulted in an increased incorporation of [3H]-thymidine, a parameter for lymphocyte activation. Activation of splenic lymphocytes with the optimal endotoxin concentration of 100 micrograms/ml for 24 hours induced a 27% decrease in the Bmax whereas the Kd for [125-I]-CYP binding was not changed. Based on these findings, we speculate that activation of lymphocytes with endotoxin in vitro and in vivo is associated with a reduction in the number of beta-adrenergic binding sites on these cells. Anterior hypothalamic (AHA) lesions protected against the endotoxin-induced reduction in the number of beta-adrenergic binding sites on lymphocytes. The protective effect of these lesions could not be related to alterations in the plasma levels of cortisol, triiodothyronine (T3), thyroxine (T4), adrenaline and noradrenaline or to splenic noradrenaline content. Since AHA lesions have been shown to inhibit several lymphocyte functions, it is suggested that these lesions prevent lymphocyte activation after in vivo endotoxin administration and through this abrogate the reduction of the beta-adrenergic binding sites.

Animals↗
PubMed1996

Endotoxin depletes ascorbate in the guinea pig heart. Protective effects of vitamins C and E against oxidative stress.

The effect of acute endotoxin-induced septic shock on myocardium oxidative stress after low or high vitamin C and/or E dietary supplementation was studied in guinea pigs, laboratory animals which, like human, do not have capacity for ascorbate synthesis. Neither the antioxidant enzymes or GSH were modified by endotoxin and vitamin treatments. Vitamin E showed a strong capacity to protect the myocardium against both enzymatic and non-enzymatic lipid peroxidation even in the presence of endotoxin. Vitamin C supplementation increased heart ascorbate whereas endotoxic shock totally depleted the heart ascorbate of vitamin C supplemented animals without changing vitamin E. Endotoxin significantly increased myocardium uric acid, a marker of ischemia induced oxidative stress, in animals fed with low vitamin C levels. This increase was totally prevented in vitamin C supplemented, but not in vitamin E supplemented animals. Strongly depressed levels of plasma vitamin C have been recently described in sepsis in human patients. The results suggest that ascorbate is a primary antioxidant target in the heart of endotoxin treated mammals lacking the capacity to synthesize ascorbate and that ascorbate can have a protective value against endotoxin-induced free radical damage in the myocardium. Implications of these results for the possible preventive role of vitamin C in humans during sepsis are discussed.

Analysis of Variance↗
PubMed1983

Role of endorphins in endotoxin-induced hyperglycaemia in mice.

The present study assessed the role of endogenous opiate systems in the hyperglycaemic response to challenge with endotoxin in mice. Blockade of opiate receptors by administration of the opiate antagonists naloxone (1.0 mg/kg) or naltrexone (1.0 or 5.0 mg/kg) significantly decreased the degree of hyperglycaemia caused by challenge with endotoxin (80 micrograms). Naltrexone methyl bromide, a peripherally acting opiate antagonist, had no demonstrable effect on the endotoxin-induced hyperglycaemia. Finally, induction of tolerance to morphine prevented the hyperglycaemic response to challenge with endotoxin. These results suggest a causative role for central endorphinergic mechanisms in the hyperglycaemic response to administration of endotoxin. They support the view that the centrally acting opiate antagonist, by blocking the brain opiate receptors, can influence metabolic adaptation to endotoxin-induced shock.

Animals↗
PubMed1995

Detection of monocyte tissue factor after endotoxin stimulation: comparison of one functional and three immunological methods.

Monocyte procoagulant activity is mainly due to tissue factor (TF) expression, but functional assays may not be sufficiently accurate in clinical use, making useful a determination of TF antigen level. The aim of this study was to compare the results of one functional and three immunological TF assays (ELISA, immunocytochemical staining on slides and flow immuno cytometric analysis), in normal monocytes, after standardized stimulation by endotoxin. TF expression was determined in blood mononuclear cells isolated by gradient centrifugation and cultured, with or without various concentrations of endotoxin. On lysed cells, TF activity was determined by amidolytic assay and TF antigen level was determined, after triton extraction, by ELISA (Imubind, American Diagnostica). Mouse monoclonal antibody against TF (4508, American Diagnostica) was used for 1) immunocytochemical (ICC) staining on cytocentrifuge slides (Avidine-Biotine-peroxidase-Complex revelation) and 2) flow cytometric analysis using indirect labeling (Fab'2 Fluoresceine Isothyocyanate revelation). The determination of TF activity and TF antigen by ELISA method were equally sensitive to low concentration of endotoxin (0.005 EU/ml) and well correlated in the presence of higher concentrations of endotoxin. ICC led to a qualitative detection with a similar sensitivity to endotoxin stimulation. Flow cytometric analysis was poorly sensitive to increasing stimulation of monocytes. Of note, the functional, ELISA and immunocytochemical assays for monocyte TF expression were sensitive to endotoxin concentrations as low as 0.005 EU/ml.

Adult↗
PubMed1980

Beneficial actions of imidazole in endotoxin shock.

The effects of imidazole were studied in anesthetized cats during endotoxin shock. Imidazole (25 mg/hg/hr) was administered 30 minutes after intravenous injection of E. coli endotoxin (5 mg/kg). The degree of the severity of the shock state was assessed by mean arterial blood pressure (MABP), and by plasma cathepsin D and MDF activities. Analysis of thromboxane B2 concentrations during shock was also performed by radioimmunoassay. Administration of imidazole to cats given endotoxin partially prevented the decrease in MABP of endotoxin shock. Imidazole significantly prevented the increase in plasma cathepsin D and MDF activities. Thus, infusion of imidazole resulted in metabolic and hemodynamic improvement during endotoxin shock. The mechanism of imidazole protection appears to be via lysosomal membrane stabilization, stimulation of cardiac function and possibly by antagonizing the biochemical effects of endotoxin administration, rather than by inhibition of thromboxane synthesis. Data obtained using imidazole to block thromboxane synthesis in shock states must be interpreted with caution.

Animals↗
PubMed1984

Interleukin 1 secretion by human monocytes stimulated by the isolated polysaccharide region of the Bordetella pertussis endotoxin.

The isolated polysaccharide chain, PS-1, of the Bordetella pertussis endotoxin was examined by isoelectric focusing, SDS-polyacrylamide gel electrophoresis and gel filtration for heterogeneity and for possible contamination by the parent endotoxin. This polysaccharide, previously found to be a very potent, macrophage-dependent, polyclonal B-cell activator and to mediate the specific binding of the endotoxin to macrophages, stimulated the interleukin 1 (IL 1) secretion by human monocytes; its potency was similar to that measured for the endotoxin. It was concluded that endotoxin-induced IL 1 production may be initiated by the interaction of the polysaccharide chain of the B. pertussis endotoxin and a specific structure present on macrophages.

Adult↗
PubMed1984

Role of vasoactive amines in the antitumor activity of endotoxin.

To estimate a possible role of vasoamines in the antitumor action of endotoxin, effects of isoproterenol, serotonin and adrenaline on subcutaneously transplanted murine Meth A sarcoma and the capacity of these agents to elicit antitumor factors were studied. Macroscopically all agents induced tumor necrosis and a temporal tumor growth stop, but only endotoxin was capable of induction of complete tumor regression. Histology showed that all agents induced hyperemia by 4 h and hemorrhagic necrosis by 24 h. The latter was located superficially at the outside of tumors. Only serotonin and especially endotoxin induced substantial non-hemorrhagic necrosis in the remaining part of the tumors. Endotoxin induced a profound inhibition of the mitotic activity within the tumor, the effect of other agents was considerably less. Only endotoxin induced high levels of tumor necrosis factor, heat stable cytostatic factors and interferon in the circulation of mice treated with Corynebacterium parvum 14 days earlier. It is concluded that these and other data provide indirect but circumstantial evidence for a role of vasoamines in the induction of hyperemia and hemorrhagic necrosis by endotoxin. The latter two effects are probably causally related. It is suggested that non-toxic vasoamines may be useful adjuvants to other treatments of cancer.

Animals↗
PubMed1989

A simple turbidimetric time assay of the endotoxin in plasma.

In order to apply the turbidimetric time assay system to the quantitative measurement of endotoxin in plasma, the optimal pretreatment of samples was investigated. After a one-tenth dilution of heparinized plasma followed by heating at 100 degrees C for 10 min, the recovery of added endotoxin was about 90% and a well correlated and reproducible standard curve was obtained in the range 10-1000 pg endotoxin per ml plasma. The amount of endotoxin present in plasma from normal subjects, thus measured, was lower than 10 pg/ml when Escherichia coli 0111:B4 endotoxin was used as a reference. It took no more than 2 h to complete the assay. High values were obtained in cases of liver cirrhosis and severe peritonitis as expected. The present method may be applied for clinical use to quantitate circulating endotoxin, because of its simplicity and high reproducibility.

Autoanalysis↗
PubMed1992

Release of tumor necrosis factor-alpha from bovine alveolar macrophages stimulated with bovine respiratory viruses and bacterial endotoxins.

The release of tumor necrosis factor-alpha (TNF-alpha) from cultured bovine alveolar macrophages (BAM) was evaluated following stimulation of BAM with bovine herpesvirus-1 (BHV-1), parainfluenza-3 (PI-3) virus, bovine respiratory syncytial virus (BRSV), Escherichia coli 0111:B4 endotoxin, Pasteurella haemolytica type 1 endotoxin, Pasteurella multocida endotoxin, and virus/endotoxin combinations. A cytotoxic assay system using Georgia bovine kidney cells as targets was used to measure TNF-alpha activity. The cytotoxic activity was neutralized by an anti-human TNF-alpha monoclonal antibody. Stimulation of BAM with 1 median tissue culture infectious dose (TCID50) of live or ultraviolet (UV)-inactivated PI-3 virus/cell resulted in release of TNF-alpha in significantly (P less than 0.05) higher amounts than sham-induced BAM. The quantities of TNF-alpha released after live or UV-inactivated BHV-1 or BRSV induction were not significantly higher than sham-induced BAM. E. coli 0111:B4, P. haemolytica type 1 and P. multocida endotoxins stimulated TNF-alpha release in a dose-dependent manner. Sequential exposure of BAM to 1 TCID50 per cell of either live BHV-1, PI-3 virus or BRSV and then 5 micrograms ml-1 of either E. coli 0111:B4, P. haemolytica type 1 or P. multocida endotoxin caused a significant (P less than 0.05) reduction in detectable TNF-alpha in seven of nine virus/endotoxin combinations tested, when compared with 5 micrograms ml-1 of endotoxin alone. Parainfluenza-3 virus/endotoxin combinations stimulated higher TNF-alpha release when compared with other virus/endotoxin combinations. Five out of six test animals had serum-neutralizing antibodies to PI-3 virus, one out of six had serum-neutralizing antibodies to BHV-1, and two out of six had serum-neutralizing antibodies to BRSV, suggesting a possible relationship between serum neutralizing antibodies and TNF-alpha release from in vitro cultivated BAM.

Animals↗