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PubMed1994

Failure of protection against endotoxin hepatotoxicity by selenium.

The present study was undertaken in rats to test the ability of selenium to prevent endotoxin hepatotoxicity. There were no significant morphological changes in the liver and no abnormalities of liver function in rats given 0, 6.25 or 12.5 mumol of selenium. Endotoxin administration to these rats induced focal hepatocellular coagulative necrosis and increased serum transaminase activities. However, endotoxin hepatotoxicity and mortality of the rats given endotoxin after treatment with 6.25 or 12.5 mumol of selenium were not significantly lower than in those given endotoxin alone. These facts suggest that selenium does not prevent endotoxin hepatotoxicity.

Animals↗
PubMed1992

Role of lipid peroxidation in enhancement of endotoxin hepatotoxicity.

The present study was undertaken in the rats to examine whether endotoxin hepatotoxicity is enhanced by increased lipid peroxidation. The rats were given 10 ml of water, corn oil or heated and oxygenated corn oil per kg body weight by stomach tube twice a day for 14 days, and then they were injected physiological saline solution or endotoxin (2 or 2.5 mg per kg body weight) into the tail vein. In the rats pretreated with water or corn oil, the activity of serum glutamic pyruvic transaminase was within the normal limit, and there was no conspicuous morphological change in the liver, except for accumulation of fine fat droplets in few liver cells. On the other hand, in the rats pretreated with heated and oxygenated corn oil, containing a large amount of lipid peroxides, accumulation of small fat droplets in the liver cells and a slight elevation of serum transaminase activity were induced. The challenge with endotoxin (2.5 mg per kg body weight) caused focal hepatocellular coagulative necrosis and a marked elevation of serum transaminase activity, irrespective of the sorts of pretreatment, and there was no significant difference in the biochemical change and the histopathological damage between the rats pretreated with water, corn oil and heated and oxygenated corn oil. These results suggest that increased lipid peroxidation does not contribute to the enhancement of endotoxin hepatotoxicity, although it is thought that carbon tetrachloride and ethanol enhance endotoxin hepatotoxicity by synergism between endotoxin and the chemicals through lipid peroxidation.

Alanine Transaminase↗
PubMed1993

Augmentation of endotoxin hepatotoxicity by zinc.

The present study was undertaken in rats to determine whether zinc protects against endotoxin hepatotoxicity and mortality. Treatment with zinc (50-200 mumol/kg body weight) alone or endotoxin (lipopolysaccharide B, Escherichia coli 026:B6, Difco, 2 mg/kg body weight) alone did not induce significant morphological changes in the liver parenchyma or any abnormalities in liver function tests. The mortality rate was 0%. In the rats pretreated with 100 mumol of zinc and then injected with endotoxin, the mortality rate, the incidence of focal hepatocellular coagulative necrosis and serum transaminase activity increased markedly. Eleven of the 12 rats pretreated with 200 mumol of zinc died within 4 h after endotoxin injection. In the rats pretreated with 50 mumol of zinc and then injected with endotoxin, there was no conspicuous change, in the mortality rate, liver function tests or morphology of the liver. These experimental data indicate that zinc increases the mortality rate in endotoxemic rats and augments biochemical and morphological evidence of endotoxin hepatotoxicity.

Animals↗
PubMedDate not supplied

Recent development of rigors during infusion of urokinase: is it related to an endotoxin?

PURPOSE: This study was undertaken to determine the prevalence of rigors associated with the use of urokinase (UK) and to assay for the presence of an endotoxin in the UK solution. PATIENTS AND METHODS: Records of 75 patients who underwent 86 UK infusions between January 1988 and July 1992 were reviewed to evaluate for the development of UK-associated rigors. A modified chromogenic limulus amebocyte lysate (LAL) test was performed to determine the presence of endotoxin in four samples of UK from lots associated with rigors, one sample of UK not associated with rigors, sterile water, nonionic contrast medium, and ionic contrast medium. RESULTS: Between January 1, 1988, and July 10, 1990, 43 patients underwent 46 UK treatments (group 1) with no documented rigors (0% prevalence). In 45 of these 46 treatments, a standard, non-pulse-spray bolus of 75,000-500,000 IU of UK (mean dose, 182,222 IU) was used. Between July 11, 1990, and July 6, 1992, 38 patients underwent 40 UK treatments (group 2). In 33 of these 40 treatments, a standard bolus was given. Five patients received a pulse-spray bolus. The mean bolus was 213,768 IU (range, 100,000-500,000 IU). Eleven group 2 patients developed rigors (28% prevalence; P = .0005 vs group 1). The chromogenic LAL tests demonstrated no endotoxin in sterile water, nonionic contrast media, or ionic contrast media. Endotoxin was detected in small concentrations in the four samples of UK associated with rigors and in the UK sample not associated with rigors. CONCLUSION: The increase in the prevalence of rigors associated with the use of UK does not appear to be related to an endotoxin in UK, since the concentration of endotoxin detected is well below the threshold pyrogenic dose in humans.

Contrast Media↗
PubMed1996

Oral endotoxin in healthy adults.

This article presents a study that measured oral endotoxin levels in healthy persons with the Limulus amoebocyte lysate microassay. Only young nonsmoking adults with a healthy dentition measured with the plaque index and a good level of oral hygiene based on a twice-daily (morning and evening) tooth-brushing regimen were admitted to this open study. Each person was required to provide two oral washings of 10 ml sterile saline solution 1 week apart. Only those volunteers without oral carriage of aerobic gram-negative bacilli were enrolled in the baseline study. A total of 15 healthy adults with a median age of 29 years (range, 25 to 43 years) were included in the trial. The mean plaque score of the group was 1.2 +/- 0.1. They all maintained a twice-daily tooth-brushing regimen unaltered throughout the sampling period. A total of 30 mouth rinses were studied. None of the samples yielded potential pathogens including aerobic gram-negative bacilli, Staphylococcus aureus and yeasts; a culturing technique based on preenrichment in nutrient medium was used. Data showed mean oral endotoxin levels of 20 ng per ml of mouth rinse; the aerobic E. coli endotoxin was used as the classical standard. This is equivalent to 1 mg of anaerobic endotoxin per ml of undiluted saliva after correcting for the 10 to 10(2) dilution factor of the mouth rinse itself and for the 10(3) times less sensitivity of anaerobic endotoxin in the Limulus amoebocyte lysate-assay. The discussion includes the physiologic and clinical benefit of the low endotoxicity of anaerobic gram-negative flora apart from the technical aspects of both culture and endotoxin assays used in the study.

Adult↗
PubMed2002

Chromatographic removal of endotoxin from protein solutions by polymer particles.

Endotoxins, constituents of cell walls of gram-negative bacteria, are potential contaminants of the protein solutions originating from biological products. Such contaminants have to be removed from solutions used for intravenous administration, because of their potent biological activities causing pyrogenic reactions. Separation methods used for decontamination of water, such as ultrafiltration, have little effect on endotoxin levels in protein solutions. To remove endotoxin from a solution of high-molecular-mass compounds, such as proteins, the adsorption method has proven to be most effective. In this review, we first introduce endotoxin-specific properties in an aqueous solution, and then provide various methods of chromatographic separation of endotoxins from cellular products using polymer adsorbents. We also provide the design of novel endotoxin-specific polymer adsorbents.

Adsorption↗
PubMed2003

Membrane cartridges for endotoxin removal from interferon preparations.

The suitability of membrane cartridges for the removal of endotoxin from both distilled water and interferon preparations was examined. The endotoxin concentrations were reduced to 4.0 and 7.3 EU/ml, respectively, when about 4000 ml of distilled water with 20 and 28 EU/ml were passed through the deoxycholate and chitosan immobilized membrane cartridges. When 200 ml of interferon preparation with endotoxin concentration more than 80 EU/ml and pH 3.9 were applied to a deoxycholate immobilized membrane cartridge at a flow-rate of 9 ml/min, the endotoxin concentration was reduced to less than 10 EU/ml. However, if an interferon preparation of 450 ml, with more than 80 EU/ml of endotoxin and pH 3.9 was applied to the chitosan immobilized membrane cartridge at a flow-rate of 18 ml/min, the endotoxin concentration was reduced to less than 10 EU/ml.

Adsorption↗
PubMed1985

The relationship between faecal endotoxin and faecal microflora of the C57BL mouse.

We studied the effect of oral selective antibiotic decontamination (SD) on the faecal endotoxin content and microflora in individual C57BL mice. Suppression of the coliform count was associated with an initial rise in faecal endotoxin concentration from 0.1 to 3.1 mg/g wet faeces during the first week of SD, which fell to 0.04 mg/g during the second week of treatment. Cessation of SD resulted in an immediate sharp increase in coliform count followed by its decline and gradual recovery to pre-treatment counts. Faecal endotoxin levels followed a parallel course. SD did not effect significantly the counts of lactobacilli, bacteroides and enterococci. It appears that the coliform population is responsible for the overall level of faecal endotoxin, and that during the initial period of SD endotoxin levels are elevated, an effect which may be mediated by antibiotic-enhanced release of endotoxin.

Amphotericin B↗
PubMed1996

Endotoxins in the blood and cerebrospinal fluid of patients with African sleeping sickness.

Endotoxin levels were measured in the blood and cerebrospinal fluid (CSF) of control individuals and 2 groups of patients with African sleeping sickness. Endotoxin levels were markedly elevated in the blood (infected groups mean endotoxin values 40.2 pg/ml and 53.8 pg/ml, compared to control 11.6 pg/ml, P < 0.0001 for both increases) and CSF (infected groups mean endotoxin values 45.8 pg/ml and 50.1 pg/ml compared to control 6.3 pg/ml, P < 0.0001 for both increases) of the patients. The levels were reduced 6 weeks following different drug treatments in the 2 groups (blood levels to mean 33.8 pg/ml and 28.5 pg/ml; CSF levels to 37.4 pg/ml and 27.0 pg/ml). The blood endotoxin values correlated with the CSF values before treatment (r = 0.74 and 0.57 for the 2 groups; P < 0.0001 for both) and after treatment (r = 0.57 and 0.56 for the 2 groups; P < 0.0001 for both). It is concluded that raised endotoxin equilibrates in the blood and CSF compartments, and may contribute significantly to the pathology of sleeping sickness.

Adolescent↗
PubMed1997

Endotoxin antibodies in African sleeping sickness.

Antibodies to the core region of endotoxin (endotoxin core antibodies, EndoCAb), which cross-react with endotoxin from a range of Gram-negative bacteria, are maintained in relative homeostasis in health, but undergo marked changes in a number of different diseases associated directly or indirectly with endotoxaemic or septicaemic states. The levels of EndoCAb IgG in the blood and cerebrospinal fluid (CSF) of 35 late-stage sleeping sickness patients and 9 control individuals were measured by ELISA. EndoCAb levels were significantly elevated in the patient blood (mean EndoCAb value 290 MU/ml cf. control 182 MU/ml, P < 0.001), and CSF (mean EndoCAb value 254 MU/ml cf. control 150 MU/ml, P < 0.001). EndoCAb IgG levels correlated with endotoxin levels in patient blood (r = 0.78, P < 0.001), but not in the CSF and were not reduced 6 weeks following chemotherapy, unlike the endotoxin levels. It is concluded that late-stage sleeping sickness is associated with chronic exposure to endotoxins from Gram-negative bacteria.

Antibodies, Bacterial↗
PubMed1997

Role of T-lymphocytes in the resolution of endotoxin-induced lung injury.

An acute neutrophilic lung injury was compared in Balb/c normal and nu/nu (nude) mice to assess the role of T lymphocytes in the resolution of acute pulmonary neutrophilic inflammation following the administration of endotoxin. Maximal neutrophilic infiltration occurred on day 1 post-endotoxin treatment and declined to near normal levels by day 5. In contrast, the percentage of lymphocytes in the bronchoalveolar lavage (BAL) fluid increased from 1.8% on day 1 post-endotoxin to greater than 11% on days three and five, during which time neutrophil resolution was occurring. On days 1-5 after endotoxin administration, approximately 40% of the CD4 lymphocytes expressed the cell surface activation marker, CD69. Despite being CD69+, CD4 cells did not express the high affinity IL-2 receptor chain, CD25, to any significant extent on any of the days studied. To assess the contribution of T cells to the rate of clearance of neutrophils from the BAL, normal and nude Balb/c mice were compared for the percentage of neutrophils following nasal administration of endotoxin. Endotoxin-treated nude mice did not demonstrate significant differences in either the total white blood cell counts or in the clearance of neutrophils from the BAL, as compared to normal Balb/c mice. These data indicate that the influx of activated T cells during the resolution of neutrophilic pneumonitis does not contribute to the rate of neutrophil clearance during acute lung injury.

Animals↗
PubMed2002

Influence of surgery and endotoxin-induced sepsis combined on natural killer cell activity, oxidative burst of granulocytes and antigen presentation capability of monocytes.

BACKGROUND: Cell mediated immunity is affected in the course of sepsis and following surgical stress. The natural killer (NK) cells, the granulocytes and the monocytes constitute the immediate unspecific cell mediated immunity. We therefore investigated the effect of surgery- and endotoxin-induced sepsis on NK cells, granulocytes and monocytes in a two-hit model. METHODS: Three groups of 40 mice. Each group was divided into four groups of 10 mice. All the animals were anesthetized and subjected to either: laparotomy; treatment with Escherichia coli endotoxin i.p.; laparotomy followed 20 min later by endotoxin i.p.; or left untreated as a control group. In the first 40 mice the NK cell activity in the spleen and number of NK cells in the liver were measured, in the second the oxidative burst of granulocytes, and in the third the antigen presentation capacity of monocytes. RESULTS: Endotoxin stimulated the NK cell activity and up-regulated the antigen presentation capability on monocytes. In contrast, surgical stress reduced the NK cell activity, the number of NK cells and down-regulated the antigen presentation capability on monocytes. After surgery, followed by administration of endotoxin, the oxidative burst of granulocytes was stimulated while antigen presentation capability on monocytes was down-regulated. Endotoxin prevented or reverted the postoperative suppression of NK cell activity. CONCLUSION: Our two-hit model shows that some cell types of the unspecific immune system exhibit an excessive inflammatory response (NK cells, granulocytes) while specific functions of other cell types (monocytes) are simultaneously diminished. This diversity makes a potential therapeutic immunomodulation very complex as some cell types would need to be down-regulated while others need to be stimulated.

Animals↗
PubMed2002

Predictors of high endotoxin concentrations in the settled dust of German homes.

Endotoxin concentrations in settled house dust were measured within the collaborative study named INGA (Indoor Exposure and Genetics in Asthma) together with other asthma-related indoor factors in 405 randomly selected homes in two German cities. Endotoxin was assayed using the quantitative kinetic chromogenic Limulus Amebocyte Lysate (LAL) method. The mean concentration of 2,274 ng endotoxin/g dust in living rooms is about two orders of magnitude below mean occupational exposure (e.g. agriculture). Endotoxin concentrations are higher in old buildings (means ratio = (MR) 1.52, 95% C.I.: 1.14; 2.04), and in the lower storey of the dwelling (MR = 1.30, 95% C.I.: 1.04; 1.62). Furthermore, higher endotoxin concentrations are associated with longer occupancy in the apartment (MR = 1.63, 95% C.I.: 1.21; 2.18), high utilisation of the apartment during the sampling period (MR = 2.52, 95% C.I.: 1.42; 4.47), infrequent vacuum cleaning of the carpets (MR = 1.67; 95% C.I.: 1.10; 2.54), an indifferent attitude to ventilation (MR = 1.37; 95% C.I.: 1.03; 1.82), keeping cats (MR = 1.91; 95% C.I.: 1.43; 2.55) and dogs (1.57; 95% C.I.: 1.08; 2.30), as well as the occurrence of mice (MR = 1.39; 95% C.I.: 1.00; 1.93). The season and indoor climate (operative temperature and relative humidity) did not effect endotoxin concentration. These results indicate that high endotoxin concentration in settled dust is an indicator of poor hygienic conditions in homes.

Adult↗
PubMed2002

Cell-specific nitric oxide synthase-isoenzyme expression and regulation in response to endotoxin in intact rat lungs.

Nitric oxide (NO) produced by NO synthase (NOS) serves as a ubiquitous mediator molecule involved in many physiologic lung functions, including regulation of vascular and bronchial tone, immunocompetence, and neuronal signaling. On the other hand, excessive and inappropriate NO synthesis in inflammation and sepsis has been implicated in vascular abnormalities and cell injury. At least three different NOS isoforms (neuronal/brain [bNOS], inducible [iNOS], and endothelial [eNOS]) have been described, which are all expressed in normal lung tissue. We investigated the cell-specific expression of bNOS, iNOS, and eNOS in perfused control rat lungs and lungs undergoing stimulation with endotoxin in the presence and absence of plasma constituents. Lung immunohistochemistry and quantitative evaluation of staining intensity showed endotoxin-induced increase in iNOS expression in particular in bronchial epithelial cells, cells of the bronchus-associated lymphoid tissue (BALT), alveolar macrophages, and vascular smooth muscle cells in a time- and dose-dependent fashion. In endothelial cells, which did not express iNOS at baseline, newly induced iNOS was found in response to endotoxin. In contrast, expression of eNOS was markedly suppressed under endotoxin challenge, particularly in bronchial epithelium, BALT, and alveolar macrophages but also in vascular smooth muscle cells and endothelial cells. eNOS expression in bronchial smooth muscle cells was not altered. In contrast to iNOS and eNOS, cellular expression of bNOS in epithelial cells, nerve fibers, BALT, and endothelial cells did not change in response to endotoxin. All changes in NOS regulation were found to be independent of plasma constituents. We conclude that endotoxin exerts a profound impact on the cell-specific NOS regulation in a large number of lung cell types. Prominent features include de novo synthesis or up-regulation of iNOS, in contrast to down-regulation of eNOS, which may well contribute to vascular abnormalities, inflammatory sequelae, and loss of physiologic functions in septic lung failure.

Animals↗
PubMed2001

A preliminary investigation of the microbiology and endotoxin content in the water reservoirs of benchtop non-vacuum autoclaves.

UNLABELLED: To determine the microbial content and endotoxin concentration in the water reservoirs of benchtop autoclaves used in general dental practice. DESIGN: The study was done in two stages. Firstly water samples were taken daily from the reservoirs of 20 autoclaves used in general dental practices for six days. The microbial content and endotoxin concentration was determined. Second the practitioners were instructed to wash and clean the reservoirs of the autoclaves each morning prior to refilling with fresh water. The reservoirs were sampled in the evenings after a day's use and the microbial content and endotoxin concentration determined. RESULTS: The total viable count of bacteria before cleaning varied from 2,300 - 8 x 10(4) cfu/ml and after from 0-40 cfu/ml. The endotoxin concentrations before cleaning varied from 360-2,200 EU/ml and after 0-80 EU/ml. CONCLUSIONS: The reservoirs of non-vacuum benchtop autoclaves can become severely contaminated with micro-organisms particularly Gram-negative bacteria. The endotoxin content of the reservoirs can get to high and unacceptable concentrations. Draining the water reservoir and cleaning on a daily basis reduces the microbial content and the endotoxin concentration to acceptable levels.

Colony Count, Microbial↗
PubMed2000

Role of central glutamate receptors, nitric oxide and soluble guanylyl cyclase in the inhibition by endotoxin of rat gastric acid secretion.

1. This study examines the role of a central pathway involving glutamate receptors, nitric oxide (NO) and cyclic GMP in the acute inhibitory effects of low doses of peripheral endotoxin on pentagastrin-stimulated acid production. 2. Vagotomy or intracisternal (i.c.) microinjections of the NO-inhibitor, N(G)-nitro-L-arginine methyl esther (L-NAME; 200 microg rat(-1)) restored acid secretory responses in endotoxin (10 microg kg(-1), i.v.)-treated rats. 3. The acid-inhibitory effect of i.v. endotoxin (10 microg kg(-1), i.v.) was prevented by prior i.c. administration of the NMDA receptor antagonists, dizocilpine maleate (MK-801; 10 nmol rat(-1)) and D-2-amino-5-phosphono-valeric acid (AP-5; 20 nmol rat(-1)), or the AMPA/kainate antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX; 10 nmol rat(-1)). However, the competitive metabotropic glutamate receptor antagonist (+)-alpha-methyl-4-carboxyphenylglycine (MCPG; 20 - 1000 nmol rat(-1)) did not antagonize the effects of endotoxin. 4. I.c. administration of L-glutamate (0.1 nmol rat(-1)) inhibited pentagastrin-stimulated gastric acid secretion. Coadministration with L-NAME (200 microg rat(-1)) prevented the inhibition of gastric acid secretion by the aminoacid. 5. I.c. administration of 1H-[1,2, 4]Oxazodiolo[4,3-a]quinoxalin-1-one (ODQ; 100 nmol rat(-1)), a soluble guanylyl cyclase (sGC) blocker, reversed the hyposecretory effect of endotoxin. 6. I.c. administration of the cyclic GMP analogue 8-Bromoguanosine-3,5-cyclic monophosphate (8-Br-cGMP; 100 - 300 nmol rat(-1)) reduced gastric acid production in a dose-dependent manner. 7. We conclude that central NMDA and AMPA/kainate receptors are involved in the acid inhibitory effect of peripherally administered endotoxin. This central pathway involves synthesis of NO, which acts on the enzyme sGC.

Animals↗
PubMed2000

Exposure to endotoxin or other bacterial components might protect against the development of atopy.

BACKGROUND: Several recent studies have shown that growing up on a farm confers significant protection against the development of atopy. These findings point particularly towards the importance of exposure to stable dust and farm animals. It has furthermore been reported that endotoxin, an intrinsic part of the outer membrane of gram negative bacteria, is abundant in environments where livestock and poultry is kept. The aim of this study was therefore to measure the level of environmental endotoxin exposure in homes of farmers' children, children with regular contact to livestock and control children with no contact to farm animals. METHODS: Eighty-four farming and nonfarming families were identified in rural areas in Southern Germany and Switzerland. Samples of settled and airborne dust were collected in stables, and of settled dust indoors from kitchen floors and the children's mattresses. Endotoxin concentrations were determined by a kinetic Limulus assay. RESULTS: Endotoxin concentrations were highest in stables of farming families, but were also significantly higher indoors in dust from kitchen floors (143 EU/mg vs 39 EU/mg, P < 0.001) and children's mattresses (49479 EU/m2 vs 9383 EU/m2, P < 0.001) as compared to control children from nonfarming families. In addition, endotoxin levels were also significantly higher in mattresses and dust from kitchen floors in households where children had regular contact to farm animals (38.6 EU/mg and 23340 EU/m2, respectively) as compared to control subjects. CONCLUSION: We propose that the level of environmental exposure to endotoxin and other bacterial wall components is an important protective determinant for the development of atopic diseases in childhood.

Adolescent↗
PubMed2003

Endotoxin levels in Estonian and Swedish house dust and atopy in infancy.

BACKGROUND: Immune responses, including those to allergens, may be T helper (Th)2 skewed in newborns. In order to redress the fetal Th1/Th2 imbalance, Th1-stimulating factors, such as bacterial endotoxin, may be required. The increasing prevalence and severity of atopic diseases in industrialized countries, which are in marked contrast with the low prevalence of allergy among children in the formerly socialist countries of Europe, have been suggested to be caused by a reduced microbial stimulation. AIM: To relate the endotoxin levels in house dust from two countries with a low (Estonia) and a high (Sweden) prevalence of allergy to the development of atopic disease and sensitization in the children during the first 2 years of life. METHODS: The study included 108 children from Tartu, Estonia and 111 children from Linköping, Sweden. Skin prick tests were performed at 3, 6, 12 and 24 months of age, and questionnaires were distributed to the families. At 24 months, a paediatrician examined the children. Dust samples were collected from mattresses and carpets and the endotoxin concentration was determined by a chromogenic Limulus assay. RESULTS: The endotoxin levels were higher in Estonian than in Swedish house dust (median levels 29 (range 0.25-280) and 14 (range 0.25-99) EU/mg dust, respectively, P < 0.001). Furthermore, the levels were inversely related to the development of atopic disease and sensitization in the Swedish, but not in the Estonian, children. CONCLUSIONS: The low prevalence of atopic disease in Estonia may, at least in part, be related to the high endotoxin levels in this country. The findings support that high levels of endotoxin, or other bacterial products with Th1-stimulating properties, might protect children from developing atopic disease.

Beds↗