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PubMed2003

Effects of endotoxin exposure on cationic amino acid transporter function in ovine peripheral blood mononuclear cells.

Rodent models of sepsis differ from clinical human disease in that humans make substantially less whole-body nitric oxide and have different cellular responses to endotoxin. Sheep, when exposed to endotoxin, behave in a manner more similar to humans. Many studies of rodent peripheral blood mononuclear cells (PBMCs) exposed to endotoxin demonstrate increased cationic amino acid transporter function (particularly through the y+ transporter) to supply arginine substrate to upregulated nitric oxide synthase. Whether this is true in sheep is not known. We have studied cationic amino acid transport in sheep PBMCs stimulated with endotoxin, using labelled lysine. PBMCs stimulated both in vitro and in vivo show an initial reduction in total and y+ lysine transport (after 1-2 h exposure to endotoxin): a previously undescribed effect of endotoxin. In in vitro activated cells, the reduction in y+ transport was prevented by the lipoxygenase inhibitor, nordihydroguaretic acid (NDGA), and the phospholipase inhibitor 4-bromophenacyl bromide (4-BPAB), but not cyclohexamide or a number of other inhibitors of intracellular second-messenger pathways. In contrast after 14 h incubation, the expected increase in total and y+ lysine transport was seen. The increase in y+ transport could be prevented by cyclohexamide, dexamethasone, ibuprofen, the protein kinase C inhibitor sphingosine, NDGA and 4-BPAB. These results suggest that in response to endotoxin exposure there is an initial decrease in y+ activity mediated by a lipoxygenase product, followed by a substantial increase in y+ activity mediated by the products of either cyclo-oxygenase or lipoxygenase. Cyclo-oxygenase and/or lipoxygenase inhibition might be useful in reducing arginine transport, and hence nitric oxide production, in these cells.

Amino Acid Transport System y+↗
PubMed1993

[Inhibitory effect of mouse antiendotoxin monoclonal antibody (E5) on hypotension induced by endotoxin and TNF-alpha].

Mouse anti-endotoxin monoclonal antibody (E5) is now under clinical trial (Phase II) in Japan by assessing clinical findings and plasma endotoxin levels. We attempted to evaluate an inhibitory effect of E5 on hypotension induced by endotoxin and TNF-alpha. Systolic blood pressure was measured with a programmable sphygmomanometer using the tail-cuff method. The mixture of endotoxin (E. coli O111:B4, Sigma, 2 micrograms/mouse) and recombinant mouse TNF-alpha (Genzyme, 8000 units) were injected into mice (ddY, 6-8-weeks-olds), and the change of blood pressure was observed for 3 hrs. The mixture significantly decreased the blood pressure to about 70% of the control. E5 (20 micrograms/mouse), which was injected 10 min before, significantly abrogated the effect of endotoxin and TNF-alpha. The hypotension induced by the mixture was definitely inhibited by the injection of E5 (50, 100 micrograms/mouse), injected 10 min later, or the injection of E5 (100 micrograms/mouse) 30 min later. We previously found that E5 prevents the lethality induced by a concomitant injection of endotoxin, TNF-alpha and IL-2. These results suggest that E5 effective for inhibition of endotoxin activity in vivo.

Animals↗
PubMed1974

Inactivation of endotoxin by polymyxin B.

The limulus gelation assay was utilized to investigate endotoxin inactivation by a number of antibiotics in vitro. Endotoxin activity was sharply reduced by polymyxin B and sodium colistimethate. The effect of the polymyxin was not significantly inhibited by 0.001 M calcium or 90% serum. Crude endotoxins from a variety of aerobic gram-negative bacteria, including several not previously studied, could be inactivated 1 or more logs by as little as 1 mug of polymyxin B per ml, whereas Bacteroides fragilis endotoxin was poorly detoxified. A 10,000-fold range in the relative susceptibility of different endotoxins to inactivation by polymyxin B was found. The endotoxin most susceptible to polymyxin B was derived from an organism resistant to polymyxin B by disk sensitivity testing, suggesting that the bacteriocidal and endotoxin detoxifying properties of polymyxin need not be directly related.

Endotoxins↗
PubMed1994

Airborne environmental endotoxin: a cross-validation of sampling and analysis techniques.

A standard method for measurement of airborne environmental endotoxin was developed and field tested in a fiberglass insulation-manufacturing facility. This method involved sampling with a capillary-pore membrane filter, extraction in buffer using a sonication bath, and analysis by the kinetic-Limulus assay with resistant-parallel-line estimation (KLARE). Cross-validation of the extraction and assay method was performed by comparison with methanolysis of samples followed by 3-hydroxy fatty acid (3-OHFA) analysis by gas chromatography-mass spectrometry. Direct methanolysis of filter samples and methanolysis of buffer extracts of the filters yielded similar 3-OHFA content (P = 0.72); the average difference was 2.1%. Analysis of buffer extracts for endotoxin content by the KLARE method and by gas chromatography-mass spectrometry for 3-OHFA content produced similar results (P = 0.23); the average difference was 0.88%. The source of endotoxin was gram-negative bacteria growing in recycled washwater used to clean the insulation-manufacturing equipment. The endotoxin and bacteria become airborne during spray cleaning operations. The types of 3-OHFAs in bacteria cultured from the washwater, present in the washwater and in the air, were similar. Virtually all of the bacteria cultured from air and water were gram negative composed mostly of two species, Deleya aesta and Acinetobacter johnsonii. Airborne countable bacteria correlated well with endotoxin (r2 = 0.64). Replicate sampling showed that results with the standard sampling, extraction, and Limulus assay by the KLARE method were highly reproducible (95% confidence interval for endotoxin measurement +/- 0.28 log10). These results demonstrate the accuracy, precision, and sensitivity of the standard procedure proposed for airborne environmental endotoxin.

Aerosols↗
PubMed1996

Mosquitocidal activity of the CryIC delta-endotoxin from Bacillus thuringiensis subsp. aizawai.

The cloned 135-kDa CryIC delta-endotoxin from Bacillus thuringiensis is a lepidopteran-active toxin, displaying high activity in vivo against Spodoptera litoralis and Spodoptera frugiperda larvae and in vitro against the S. frugiperda Sf9 cell line. Here, we report that the CryIC delta-endotoxin cloned from B. thuringienesis subsp. aizawai HD-229 and expressed in an acrystalliferous B. thuringiensis strain is also toxic to Aedes aegypti, Anophles gambiae, and Culex quinquefasciatus mosquito larvae. Furthermore, when solubilized and proteolytically activated by insect gut extracts, CryIC is cytotoxic to cell lines derived from the first two of these dipteran insects. This activity was not observed for two other lepidopteran-active delta-endotoxins, CryIA(a) and CryIA(c). However, in contrast to the case with a lepidopteran and dipteran delta-endotoxin cloned from B. thuringiensis subsp. aizawai IC1 (M.Z. Haider, B. H. Knowles, and D. J. Ellar, Eur. J. Biochem. 156:531-540, 1986), no differences in the in vitro specificity or processing of CryIC were found when it was activated by lepidopteran or dipteran gut extract. The recombinant CryIC delta-endotoxin expressed in Escherichia coli was also toxic to A. aegypti larvae. By contrast, a second cryIC gene cloned from B. thuringiensis subsp. aizawai 7.29 (V. Sanchis, D. Lereclus, G. Menou, J. Chaufaux, S. Guo, and M. M. Lecadet, Mol. Microbiol. 3:229-238, 1989) was nontoxic. DNA sequencing showed that the two genes were identical. However, CryIC from B. thuringiensis subsp. aizawai 7.29 had been cloned with a truncated C terminus, and when it was compared with the full-length CryIC delta-endotoxin, it was found to be insoluble under alkaline reducing conditions. These results show that CryIC from B. thuringiensis subsp. aizawai is a dually active delta-endotoxin.

Aedes↗
PubMed1979

Suppressive effect of bacterial endotoxin on the expression of cell-mediated anti-Listeria immunity.

Intravenous injection of bacterial endotoxin into mice at any time during ongoing infection with Listeria monocytogenes resulted in a markedly increased multiplication of this organism in the liver and spleen. Experiments designed to investigate the basis of this infection-enhancing effect revealed that endotoxin was also capable of inhibiting the expression of adoptive T-cell-mediated anti-Listeria immunity if given to normal recipient mice up to 48 h before they were infused with protective T-cells. On the other hand, endotoxin had only a marginal effect on the expression of adoptive immunity if given to donor mice before their spleen cells were harvested for adoptive transfer. Taken together, these results indicate that endotoxin probably interferes with the antibacterial function of macrophages rather than with mediator lymphocytes. The additional finding that the infection-enhancing action of endotoxin could be greatly reduced by making mice "tolerant" to endotoxin suggests that the acquisition of tolerance to this effect of endotoxin may be an important adaptive mechanism in acquired resistance to infection with gram-negative bacteria.

Animals↗
PubMed1983

Down regulation of hepatic glucocorticoid receptors after endotoxin treatment.

The mechanism by which endotoxin administration results in hypoglycemia was evaluated by characterizing [3H]dexamethasone binding and phosphoenolpyruvate carboxykinase activity in hepatic cytosol preparations from treated and control mice. Starved mice were given Escherichia coli O111:B4 endotoxin or saline intraperitoneally on day 3 after bilateral adrenalectomy. [3H]dexamethasone binding was measured by the charcoal method after the incubation of cytosol preparations with [3H]dexamethasone in the presence or absence of unlabeled dexamethasone. Changes in [3H]dexamethasone binding were found to be time and dose dependent in treated mice. When mice given different doses of endotoxin reached the same stage of morbidity, as indicated by the average time of death, significantly lower glucocorticoid binding was measured. Scatchard analysis of binding isotherms defined a single class of binding sites. Association and dissociation rate constants and the equilibrium dissociation constant (Kd) were not altered, but the maximum number of binding sites was depressed by endotoxin. The rank order of potency of competitors for [3H]dexamethasone binding, dexamethasone greater than hydrocortisone = corticosterone greater than deoxycorticosterone greater than progesterone greater than testosterone = estradiol, was consistent with a glucocorticoid receptor, although the competition was not altered by endotoxin. Endotoxin treatment prevented the glucocorticoid-induced increase in hepatic phosphoenolpyruvate carboxykinase activity. We conclude that the hypoglycemia of endotoxin poisoning is effected, in part, by the inhibition of the glucocorticoid-mediated induction of phosphoenolpyruvate carboxykinase via the down regulation of hepatic glucocorticoid receptors.

Animals↗
PubMed1984

A Cytophaga species endotoxin as a putative agent of occupation-related lung disease.

A previous study suggested that a biologically active bacterial endotoxin was a putative agent of lung disease in a textile-producing facility. The endotoxin was isolated from the biomass growing in a chilled-water spray air humidification system. The bacterial flora of the air humidification system were isolated and taxonomically identified to the genus level. By using indirect immunofluorescence assays, a serologically reactive Cytophaga species was identified. A serologically reactive, biologically active (Limulus assay) endotoxin was purified from phenol extracts of the Cytophaga species. The endotoxin contained sugars, hexosamines, and lipids identical to those found in the humidifier biomass endotoxin. All subjects with biopsy-proven and suspected lung disease had antibodies directed toward the purified Cytophaga endotoxin. The data suggest that the Cytophaga endotoxin is the putative agent of lung disease in the textile facility.

Bacterial Infections↗
PubMed1984

Endogenous interferon production by endotoxin-responsive macrophages provides an autostimulatory differentiation signal.

Previous studies have demonstrated that peritoneal macrophages (resident or thioglycolate-induced) derived from mouse strains fully responsive to gram-negative endotoxins continue to differentiate in vitro, as evidenced by an increased capacity to phagocytose via the Fc receptor with time in culture. In contrast, macrophages derived from endotoxin-hyporesponsive mouse strains (e.g., C3H/HeJ or C57BL/10ScN) exhibit no such increase in phagocytic capacity, and, in fact, significantly lose the capacity to phagocytose particles opsonized with immunoglobulin G with time in culture. This defect was found to be fully correctable by the addition to the cultures of an exogenous source of alpha, beta, or gamma interferon. In this study, we compared C3H/HeN (endotoxin-responsive) and C3H/HeJ (endotoxin-responsive) and C3H/HeJ (endotoxin-hyporesponsive) macrophages in an attempt to elucidate the mechanism responsible for this difference in phagocytic (differentiative) potential. The following observations support the hypothesis that endotoxin-responsive macrophages, in contrast to endotoxin-hyporesponsive macrophages, produce significantly higher levels of an autostimulatory differentiation signal that appears to be macrophage-derived interferon. (i) Anti-alpha/beta-interferon antibody greatly reduces the ability of C3H/HeN macrophages to phagocytose opsonized erythrocytes: (ii) C3H/HeJ macrophages can be made more phagocytic by coculture with C3H/HeN macrophages or by treatment with supernatants derived from C3H/HeN macrophage cultures; and (iii) C3H/HeN macrophages spontaneously lose Mac-1 antigen with time in culture. C3H/HeJ macrophages must be interferon-treated to be equivalently down-regulated.

Animals↗
PubMed1972

Carbohydrate metabolism and survival of endotoxin-poisoned mice given tryptophan.

Severe hypoglycemia and increased deaths were observed among two strains of endotoxin-poisoned mice within 3 to 6 hr after tryptophan injection. Sensitivity to tryptophan could be demonstrated in Rockland Farms mice by 4 hr after endotoxin and in Carworth Farms (CF-1) mice by 10 hr after endotoxin. If allopurinol was given to CF-1 mice concurrently with endotoxin, severe hypoglycemia and increased deaths were observed when tryptophan was given only 4 hr after the bacterial poison. Cyproheptadine, an antiserotonin drug, decreased the number of deaths as well as the depletion of blood glucose in both strains of endotoxin-poisoned mice given a delayed injection of tryptophan. In most instances, liver glycogen was depleted by 8 to 10 hr after endotoxin. Correlation of liver glycogen levels with sensitivity to tryptophan was not as consistent as the correlation between blood glucose levels and hyperreactivity to the amino acid. The data show that severe hypoglycemia is a significant factor which must be considered in resolving the basis for increased deaths among endotoxin-poisoned mice given tryptophan.

Allopurinol↗
PubMed1996

Influence of endotoxin on daytime sleep in humans.

Administration of endotoxin in the evening has been shown to transiently suppress rapid eye movement (REM) and to promote non-REM sleep in humans. In a single-blind placebo-controlled crossover design, we assessed the effects of Salmonella abortus equi endotoxin administered intravenously in the morning on the primary host response and on daytime sleep by use of a multiple napping protocol in healthy volunteers. The extent of the host response achieved by 0.8 ng of endotoxin per kg of body weight given at 0900 h was comparable to that previously reported to result from the administration of 0.4 ng/kg at 1900 h. However, sleep was only slightly influenced. Endotoxin reduced the amount of REM sleep and increased REM latency. Non-REM sleep amount in the first nap, although not significantly changed, correlated negatively with the individual peak levels of interleukin-6 (r = -0.73, P < 0.05). Subjective tiredness, sleep onset latency, total sleep time, and the amounts of slow-wave and non-REM sleep were not affected by endotoxin throughout the entire experiment. Spectral analysis of the electroencephalogram obtained during non-REM sleep yielded no condition differences. We conclude that endotoxin administration in the morning to healthy volunteers, while activating the host defense to the same extent as a lower dose that has been reported to promote non-REM sleep when given in the evening, does not affect non-REM sleep. REM sleep suppression is, to date, the most consistently reported effect of endotoxin on human sleep.

Adult↗
PubMed2000

Synergistic epithelial responses to endotoxin and a naturally occurring muramyl peptide.

We have investigated the synergistic interactions of a naturally occurring peptidoglycan fragment (muramyl peptide) and bacterial endotoxin in the induction of inflammatory processes within respiratory epithelial cells, at the levels of both signal transduction events and ultimate cellular metabolic effects. The source of the muramyl peptide is Bordetella pertussis, the causative agent of the respiratory disease pertussis. During log-phase growth, B. pertussis releases the muramyl peptide tracheal cytotoxin (TCT), which has the structure N - acetylglucosaminyl - 1,6 - anhydro - N - acetylmuramyl - (L) - alanyl - gamma - (D) - glutamyl - meso - diaminopimelyl - (D) - alanine, equivalent to a monomeric subunit of gram-negative bacterial peptidoglycan. When applied to hamster trachea epithelial (HTE) cells, TCT and endotoxin were found to be highly synergistic in the induction of interleukin-1alpha (IL-1alpha), type II (inducible) nitric oxide synthase (iNOS), nitric oxide production, and inhibition of DNA synthesis. Neither molecule alone significantly triggered these responses. The serine/threonine protein kinase inhibitor H7 blocked induction of both IL-1alpha and iNOS. More selective inhibitors of protein kinase C, cyclic AMP-dependent protein kinase, and cyclic GMP-dependent protein kinase were not capable of blocking the effects of TCT and endotoxin, suggesting that the H7-inhibited component in this pathway is not among the commonly described kinase targets of H7. Treatment of HTE cells with exogenous IL-1 reproduced the induction of iNOS and DNA synthesis inhibition caused by TCT and endotoxin. H7 was not capable of interfering with effects caused by exogenous IL-1, implying that the H7-sensitive step in the pathway is upstream of IL-1 protein production. Similar assays with the phorbol ester phorbol myristate acetate indicate that it could effectively synergize with endotoxin but not with TCT, suggesting that TCT and endotoxin induce different signal transduction events that combine synergistically. The synergy observed with TCT and endotoxin in epithelial cells is significantly different from their interaction with other cell types, revealing a unique inflammatory response by epithelial cells to these natural bacterial products.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1965

Some metabolic aspects of tolerance to bacterial endotoxin.

Berry, L. Joe (Bryn Mawr College, Bryn Mawr, Pa.), and Dorothy S. Smythe. Some metabolic aspects of tolerance to bacterial endotoxin. J. Bacteriol. 90:970-977. 1965.-The tolerance to bacterial endotoxins which is produced in mice given a series of daily injections of heat-killed Salmonella typhimurium failed to occur when actinomycin D was administered with the heat-killed cells. Neither ethionine nor 2-thiouracil, when given with endotoxin, altered the development of tolerance. An injection of endotoxin, actinomycin D, or ethionine lowered the activity of the liver enzyme tryptophan pyrrolase more significantly at either 4 or 17 hr postinjection in normal mice than in tolerant mice. Similarly, an injection of either saccharated iron oxide or Thorotrast lowered liver tryptophan pyrrolase activity more extensively in normal than in tolerant animals. Activation of the reticuloendothelial system (RES) of tolerant mice, as determined by an accelerated rate of carbon clearance from the blood, was observed, but this was prevented by the appropriate dose of actinomycin D. Similar results were obtained when saccharated iron oxide, rather than endotoxin, was used to activate the RES, but these animals were not resistant to endotoxin and their tryptophan pyrrolase was normally diminished after an injection of endotoxin. Thus, RES activation may occur without tolerance developing. A more nearly normal level of enzyme activity appears to be characteristic of the tolerant state.

Cortisone↗
PubMed1966

Relation of polysaccharide content to some biological properties of endotoxins from mutants of Salmonella typhimurium.

Kessel, R. W. I. (Rutgers, The State University, New Brunswick, N.J.), Henry H. Freedman, and Werner Braun. Relation of polysaccharide content to some biological properties of endotoxins from mutants of Salmonella typhimurium. J. Bacteriol. 92:592-596. 1966.-Endotoxins were extracted by the phenol-water procedure from a variety of Salmonella typhimurium mutants with known differences in the composition of their cell wall polysaccharides. The lethality of these preparations for mice proved to be correlated with the complexity of the polysaccharide: endotoxin from the smooth parent strain and from rough strains with several sugars attached to the heptose-phosphate backbone were of high toxicity, whereas endotoxin from a mutant possessing only glucose attached to the heptose-phosphate backbone was less toxic, and endotoxin from a mutant possessing the backbone only was least toxic. All of these mutants yielded endotoxins that were equally capable of protecting mice against subsequent challenge with Pseudomonas aeruginosa. Material obtained from a heptoseless mutant by the phenol-water method proved to be neither toxic nor protective. The apparent dissociation of biological properties that can be achieved with the aid of endotoxin preparations from certain mutants is discussed in terms of possible mechanisms.

Animals↗
PubMed1966

Alteration and restoration of endotoxin activity after complexing with plasma proteins.

Rudbach, Jon A. (The University of Michigan, Ann Arbor), and Arthur G. Johnson. Alteration of endotoxin activity after complexing with plasma proteins. J. Bacteriol. 92:892-898. 1966.-A substantial decrease in the ability of endotoxin to be precipitated by homologous antiserum and to cause fever occurred after incubation with human plasma or human plasma, Cohn fraction IV-1. The endotoxin, thus altered, also displayed decreased lethality for rabbits. These alterations in endotoxin activity could be restored when the endotoxin-plasma protein mixture was treated with a proteolytic enzyme, and the endotoxin was precipitated with ethyl alcohol. Inactivation of the antigenic and toxigenic properties of the endotoxin molecule by plasma is discussed as resulting from complexing with plasma proteins rather than from enzymatic degradation.

Animals↗
PubMed1967

Biologically active endotoxins from Salmonella mutants deficient in O- and R-polysaccharides and heptose.

Well-characterized Salmonella mutants formerly used in biosynthetic studies of lipopolysaccharides were used to study the toxic portion of the complex endotoxin. Endotoxins prepared from wild types and their mutants were tested for their biological activities, including pyrogenicity, lethality, and immunogenicity. There was little difference either in the endotoxin yields or in the toxicities between endotoxins from the wild-type and O-antigen deficient mutants. Endotoxin containing mostly lipid A and keto-deoxyoctonate (KDO) prepared from the mutant deficient in both O- and R-antigens and the backbone sugar, heptose, was biologically active. Possibly because of the difference in solubility in water, the yield of endotoxin from the heptoseless mutant was about 10% of the wild type. There was complete reciprocal cross-immunity between all endotoxins tested. These observations suggest that the common toxic moiety is not present in the O- and R-polysaccharides or the backbone sugar heptose, but rather is associated with the lipid portion of the molecule which includes mostly lipid A and KDO.

Animals↗
PubMed1988

New microassay for quantitation of endotoxin using Limulus amebocyte lysate combined with enzyme-linked immunosorbent assay.

A combined method of the Limulus amebocyte lysate (LAL) test and the enzyme-linked immunosorbent assay for quantitation of endotoxin was developed based on our observation that the antigenicity of coagulogen, a major protein in LAL, was lost when LAL reacted with endotoxin as shown by immunoblotting. Determination of the residual coagulogen by an enzyme-linked immunosorbent assay system with monoclonal antibody against coagulogen revealed that the loss of the antigenicity of coagulogen was proportional to the concentration of endotoxin. An inverse linear curve was established between the endotoxin concentration and absorbance. Standard curves of the LAL enzyme-linked immunosorbent assay with different detection limits (from 0.1 to 100 pg of the control standard endotoxin per ml) were obtained from one batch of commercial LAL by adjusting incubation time and dilution of LAL. The reaction curves of various endotoxins were parallel to one another, whereas the kinetics differed from that of (1-3)-beta-D-glucan. The LAL enzyme-linked immunosorbent assay is a highly reproducible microassay, using only 10 microliter of test sample and LAL reagent; because the color and turbidity of plasma samples do not interfere with the assay, it is well suited for quantitation of endotoxins in clinical specimens.

Animals↗
PubMed1989

Endotoxin removal by end-line filters.

Four commonly used end-line filters, one with a charge-modified hydrophilic nylon filter (ELD96; Pall Biomedical Ltd., Portsmouth, United Kingdom), one with an unmodified nylon filter (FAE020; Pall Biomedical), and two with hydrophilic cellulose ester filters (Ivex-HP, Millipore Corp., Bedford, Mass.; Sterifix, Braun-Gelman, Brussels, Belgium), were evaluated for their endotoxin-removing capacity in saline and 5% glucose. Natural endotoxins derived from Escherichia coli 8739 and the lipopolysaccharide mutant Pseudomonas aeruginosa PA220-R2 and a purified E. coli serotype O111:B4 lipopolysaccharide preparation were used to challenge the four end-line filters. No endotoxin-removing capacity was observed for the Ivex-HP and Sterifix filters. Both the FAE020 and the ELD96 end-line filters showed excellent endotoxin-eliminating capacities in 5% glucose. Increasing the NaCl concentration in 5% glucose, however, greatly reduced the endotoxin-removing efficiency of especially the ELD96 filter for the purified E. coli lipopolysaccharide preparation. Obviously, both the nature of the endotoxin and the ionic strength of the solution had a major influence on the endotoxin end-line filtering efficiency.

Endotoxins↗