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PubMed1996

Digestion of delta-endotoxin by gut proteases may explain reduced sensitivity of advanced instar larvae of Spodoptera littoralis to CryIC.

The present study describes the correlation between gut protease activity of lepidopteran larvae of different instars, the inactivation of Bacillus thuringiensis delta-endotoxins in crystalline and noncrystalline forms, and the reduced susceptibility of advanced larval instars of Spodoptera littoralis to the toxin. The original assembly of delta-endotoxins in a crystal structure is essential for causing efficient larval mortality. Denaturation and renaturation (D/R) of delta-endotoxin crystals increased the vulnerability of the toxin molecules to proteolysis, reduced their capability to kill neonate larvae of S. littoralis, but sustained most of their larval growth-inhibition activity. E. coli-produced CryIC delta-endotoxin applied as a fraction of inclusion bodies exerted a growth inhibition effect, similar to the molecules released from the crystals by denaturation and subsequent renaturation. Incubation of CryIC with gut juice of 1st or 2nd instar larvae, left part of the CryIC toxin intact, while the toxin was completely degraded when incubated with gut juice of 5th instar larvae. The degradation rate was consistent with the increase of protease specific activity of the gut juice during larval development. This increase in toxin degradation may account for the loss of sensitivity of 5th instar larvae to CryIC. Specific protease inhibitors such as PMSF and Leupeptin were shown to inhibit gut proteases activity in all instar larvae, while, 1,10 phenanthroline, TLCK and TPCK were effective only in young instar larvae. The differential effect of protease inhibitors on proteases obtained from different larval instars indicated that gut juice protease profiles change with larval age. The observed quantitative and qualitative differences in degradation of delta-endotoxin by larval gut proteases that occur during larval maturation may account for the difference in susceptibility to the delta-endotoxin. This finding should be taken into consideration when designing strategies for the development of transgenic crops expressing delta-endotoxins as potent insecticidal proteins.

Animals↗
PubMed2005

Endotoxin adsorbent using dimethylamine ligands.

Various adsorbents have been investigated for removing endotoxin from protein solutions. It is believed that electrostatic interaction and hydrophobic intermolecular interaction are the main interactions in adsorption of endotoxin. In this work, a series of novel molecular recognition adsorbents for removal of endotoxin with dimethylamine ligand were prepared by coupling ligands on polymethyl methacrylate. We found that its adsorption capacity of endotoxin increased almost 8 times in the presence of a hydroxyl group at beta-site of ligand. The computer simulation showed that the hydroxyl group at beta-site could form H bond with endotoxin, as a result an octatomic ring was formed. The spacer in adsorbent and the long alkyl chain in endotoxin were located at the same side of the octatomic ring. In this situation, electrostatic interaction, H bond, cooperative effect of octatomic ring and hydrophobic intermolecular interaction effected simultaneously. The combination of endotoxin with adsorbent was tight and adsorption capacity was effectually increased.

Adsorption↗
PubMed2006

Preventive effects of a biscoclaurine alkaloid, cepharanthine, on endotoxin or tumor necrosis factor-alpha-induced septic shock symptoms: involvement of from cell death in L929 cells and nitric oxide production in raw 264.7 cells.

The preventive effects of cepharanthine, a biscoclaurine alkaloid isolated from Stephania cepharantha Hayata, on the lethality and cell death caused by endotoxin or tumor necrosis factor (TNF)-alpha-induced syndrome in septic shock were investigated. In these experiments, we estimated the survival of mice treated with a lethal dose of endotoxin (50 mg/kg, i.p.) or recombinant human (rh) TNF-alpha (10,000 units/mouse, i.v.) together with a sublethal dose (1 mg/kg, i.p.) of endotoxin. Cepharanthine clearly protected mice from endotoxin-induced and endotoxin/rhTNF-alpha-induced lethal shock. In in vitro experiments, cepharanthine (3 micro g/ml) definitely inhibited cell death in mouse L929 fibroblast cells incubated with rhTNF-alpha (100 units/ml) at 37 degrees C for 24 h. On the other hand, non-apoptotic programmed death of cells was observed by fluorescence microscopy in rhTNF-alpha (100 units/ml)-treated L929 cells. In the 3-(4,5-Dimethylthiazol-2-yl) 2,5-diphenyltetrazolium bromide (MTT) assay after 48-h drug exposure, the cell proliferation of L929 cells was significantly increased by the addition of cepharanthine (1 and 3 micro g/ml). It seems that the preventive effect of cepharanthine on rhTNF-alpha-induced cytotoxicity in fibroblast cells occurs through an increase of cell proliferation by the drug. In addition, cepharanthine suppressed nitric oxide (NO) production by endotoxin-stimulated Raw 264.7 mouse macrophage cells. These findings suggest that cepharanthine prevents lethality or cytotoxicity through suppression of endotoxin-induced NO in macrophages and that its effects are possibly mediated by the enhancement of the proliferation of fibroblast cells. Cepharanthine may therefore protect against some of the various disturbances caused by endotoxin through its ability to inhibit NO production in septic shock.

Alkaloids↗
PubMed2006

Simultaneous metal chelate affinity purification and endotoxin clearance of recombinant antibody fragments.

Endotoxins are frequent contaminants of recombinant proteins produced in Escherichia coli. Due to their adverse effects, endotoxins have to be removed from recombinant proteins prior their use in cell-based assays or parenteral application. Reduction of endotoxin to less than 10 EU mg(-1) is, however, one of the most problematic steps during protein purification from E. coli and often associated with substantial loss of biological materials. The present paper describes the use of a single step procedure enabling metal chelate affinity purification and endotoxin clearance from antibody fragments produced in E. coli using a non-ionic detergent. Endotoxin content was as low as 5 to 9 EU mg(-1) with a recovery of antibody fragments of over 90%. Non-ionic detergent treatment did not compromise integrity and functionality of these multimeric molecules. Furthermore, recombinant antibody fragments did not stimulate endotoxin-sensitive cell lines confirming the low endotoxin content. In conclusion, this one-step protocol is a rapid, cost effective and automation-compatible procedure suitable for recombinant antibody fragments.

Antibodies, Monoclonal↗
PubMed2005

Induced nitric oxide impairs relaxation but not contraction in endotoxin-exposed rat pulmonary arteries.

BACKGROUND: Many patients with severe acute lung injury do not respond to nitric oxide (NO) inhalational therapy with alleviation of pulmonary arterial hypertension and hypoxemia, so this treatment remains controversial. MATERIALS AND METHODS.: We investigated in endotoxin-exposed Wistar rat pulmonary arteries whether endogenous NO alters contractile and relaxing responses, by electrochemical NO and isometric force measurements. RESULTS: Receptor-independent contraction was similar in control and endotoxin-exposed arteries, while thromboxane analogue (TxA)-dependent contraction was less in the latter. Neither non-selective NO synthase (NOS) inhibition by N(G)-nitro-l-arginine (l-NA) or selective inducible-NOS2 inhibition by aminoguanidine (AG) improved TxA-induced contraction in endotoxin-exposed arteries. Acetylcholine-induced relaxation was impaired in endotoxin-exposed pulmonary arteries, despite a comparable acetylcholine-induced NO release in control arteries. Additionally, NO solution-induced relaxation of endotoxin-exposed arteries was impaired, but could be improved by l-NA or AG. Application of a phosphodiesterase-insensitive cyclic guanosine monophosphate analogue induced similar relaxation in both control and endotoxin-exposed arteries. CONCLUSIONS: Endotoxin-associated NOS2-derived NO is thus associated with impaired NO-mediated relaxation, but does not underlie reduced receptor-mediated pulmonary contractile responses. An increased phosphodiesterase activity may underlie the former, so this route can be explored to replace or improve the effect of inhalational NO therapy in severe sepsis-induced acute lung injury in patients.

Acetylcholine↗
PubMed2005

Elevated lung cancer risk shortly after smoking cessation: is it due to a reduction of endotoxin exposure?

Several reports indicate that the risk of lung cancer increases slightly for a short period of time after cessation of smoking while the risk of adverse cardiovascular events drops immediately. Recent studies on subjects occupationally exposed to organic dust-containing endotoxin have revealed lower than expected rates of lung cancer. There is experimental evidence that stimulation of the immune system by endotoxin has a protective effect against cancer. Tobacco smoke has been shown to contain high levels of endotoxin. We therefore postulate that cessation of smoking eliminates the protective effect of endotoxin. Any benefit conferred by endotoxin does not, however, justify smoking. As the inverse relationship between exposure to endotoxin and the risk of lung cancer is a strong one, endotoxin-like substances could form the basis of vaccination strategies.

Endotoxins↗
PubMed2006

Involvement of calcium/calmodulin-dependent protein kinase II to endotoxin-induced vascular hyporeactivity in rat superior mesenteric artery.

Endotoxin causes impaired vascular contractility proposed to be mediated mainly by induction of inducible nitric oxide synthase (iNOS). Evidence suggests that calcium/calmodulin dependent protein kinase II (CaMKII) may lead to activation of cytosolic phospholipase A(2alpha) (cPLA(2alpha))/inducible cyclooxygenase (COX-2) pathway in response to endotoxin in vascular smooth muscle cells. This study was conducted to determine if CaMKII is involved in the endotoxin-induced vascular hyporeactivity by activating of iNOS and/or cPLA(2alpha)/COX-2 enzymes in rat isolated superior mesenteric artery with endothelium. Incubation with endotoxin (100 microg ml(-1)) for 4h caused vascular hyporeactivity to norepinephrine which was completely abolished by phenylene-1,3-bis[ethane-2-isothiourea] dihydrobromide (1,3-PBIT), a selective iNOS inhibitor, methyl arachidonyl fluorophosphonate (MAFP), a selective 85kDa cPLA(2alpha) inhibitor, DFU, a selective COX-2 inhibitor, and KN-93, a selective CaMKII inhibitor. Endotoxin-induced increase in tissue nitrite production was decreased by 1,3-PBIT and DFU, and further increased by MAFP. MAFP, DFU and KN-93 reversed the endotoxin-induced decrease in tissue 6-keto-PGF(1alpha). These data suggest that reversal of the endotoxin-induced vascular hyporeactivity by inhibition of CaMKII in rat superior mesenteric artery may be related to increased production of vasodilator arachidonic acid products by cPLA(2alpha)/COX-2 pathway rather than prostacyclin and nitric oxide.

6-Ketoprostaglandin F1 alpha↗
PubMed2004

A profile of the immediate endocrine, metabolic and behavioural responses following a dual exposure to endotoxin in early life.

Dual exposure to endotoxin on postnatal days (PNDs) 3 and 5 is increasingly being used to model the impact of bacterial challenge, in early life, on long-term health outcomes. Currently, however, little is known about how exposure to endotoxin using this model disrupts systems known to program physiological alterations in later life. The aim of the current study was to define, in Fischer 344 rat pups, a framework of the immediate endocrine, metabolic, and behavioural consequences following challenge with 0.05 mg/kg of endotoxin (Salmonella enteritidis) on PNDs 3 and 5. Circulating corticosterone in endotoxin challenged neonates was significantly elevated at all time points assessed on PND 3 (P<0.05), however, by PND 5 this response was attenuated showing a significant elevation only at 4-h post-injection. In these same pups, glucose levels were significantly reduced by 8-h post-injection on PND 3 and remained significantly lower until 8-h post-injection on PND 5 (P<0.05). Finally, the dams of endotoxin challenged pups, exhibited significantly less arched back nursing (P<0.05) but increased levels of off-nest time across the challenge period (P<0.05). These findings demonstrate that postnatal endotoxin exposure impacts on both endocrine and metabolic activity and that alterations in these two systems may in part be mediated by the impact of endotoxin exposure on maternal behaviour.

Age Factors↗
PubMed1996

The role of ADP in endotoxin-induced equine platelet activation.

We have shown previously that endotoxin induces platelet aggregation in equine heparinised whole blood in a platelet-activating factor (PAF; 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine) dependent manner. ADP is an agonist of platelets and is present in platelet dense granules with ATP in high concentrations. An investigation was carried out to establish whether endotoxin-induced platelet activation was associated with release of platelet ATP and ADP. ADP-scavenging enzyme systems significantly inhibited endotoxin-induced aggregation. Plasma levels of adenine nucleotides were measured using a luminometric assay following incubation of heparinised equine whole blood with endotoxin (300 ng/ml). After addition of endotoxin ATP and ADP were released from the platelets and then subsequently degraded to AMP. WEB2086 (4-[3-[4-(o-chlorophenyl)-9-methyl-6H-thieno[3,2-f]-s-triazolo[4,3-a][1, 4] diazepin-2-yl]proprionyl]-morpholine) (100 nM), a competitive PAF receptor antagonist, inhibited endotoxin-induced aggregation and also inhibited the release of adenine nucleotides from the platelets. It is concluded that endotoxin-induced aggregation is dependent upon ADP released from platelet dense granules.

Adenosine Diphosphate↗
PubMed1998

Platelet-activating factor receptor antagonist attenuates endotoxin-induced vascular hyporeactivity in the pithed rat.

The role of platelet activating factor (PAF) and nitric oxide (NO) in the endotoxin-induced hyporeactivity to noradrenaline was studied in the pithed rat. Pressor dose-response curves to noradrenaline (0.01-10 microg/kg, i.v.) were made starting 1 h after the administration of endotoxin (0.5 mg/kg, i.v.) to the rats. Saline was administered to the control rats. The PAF receptor antagonist, TCV-309 (3-bromo-5-[N-phenyl-N-[2-[[2-(1,2,3,4-tetrahydro-2-isoquinolylcarbon yloxy)ethyl]carbamoyl]ethy]carbamoyl]-1-propylpyridinium nitrate, 100 microg/kg, i.v.), or the NO synthase inhibitor, N(G)-monomethyl-L-arginine (L-NMMA, 30 mg/kg, i.v.), was administered to the endotoxin-treated rats 20 or 10 min before the noradrenaline challenge. L-NMMA reversed endotoxin-induced hyporeactivity completely. TCV-309 produced a significant, but partial attenuation of the hyporeactivity to noradrenaline (P < 0.01). There was still significant hyporeactivity when compared with the control rats (P < 0.01) and the L-NMMA-treated endotoxin-administered rats (P < 0.05). These data suggest that endogenous PAF contributes to the vascular hyporeactivity to noradrenaline induced by endotoxin and that NO plays a major role in the endotoxin-induced hyporeactivity.

Animals↗
PubMed1995

Endotoxin induced uveitis in the mouse: susceptibility and genetic control.

Endotoxin induced uveitis in the mouse provides a useful animal model for acute anterior uveitis in humans. We have investigated the susceptibility of endotoxin-induced uveitis among various mouse strains, and have examined the relationship between genetic background and the resultant inflammatory response to endotoxin. We studied ten strains with differing major histocompatibility-2 genes, lipopolysaccharide response gene, and strains with mast cell depletion and its sham control. Anterior uveitis was induced by injecting 300 micrograms of Salmonella typhimurium endotoxin into one hind footpad. Mice were then killed 8, 12, 16, 20, 24, 48 and 72 hr after endotoxin injection, and vertical sections of the eyes through the pupil-optic nerve axis were evaluated for ocular inflammation. C3H/HeN mice developed severe uveitis. In contrast, C3H/HeJ mice (lipopolysaccharide response gene-) did not develop uveitis even though it has the same genetic background and shares the same major histocompatibility-2 haplotype with C3H/HeN mice (lipopolysaccharide response gene+). The strain that was mast-cell deficient (W/Wv) developed minimal uveitis; however, W/+ mice, with mast cells, developed more inflammation at 48 and 72 hr after endotoxin injection. C3H.SW and FVB/N mice also developed severe uveitis, and BALB/C, CBA/J, and B10.A developed mild uveitis. In conclusion, there is a wide variation in the magnitude and susceptibility to endotoxin among mouse strains. Multiple factors appear to influence this variability, including non-histocompatibility-2 genetic background, the lipopolysaccharide response gene, and the presence of mast cells.

Animals↗
PubMed1998

Endotoxin tolerance does not alter open field-induced fever in rats.

Exposure to an open field has been shown to cause a rise in the body temperature of rats. In many respects, this rise in body temperature is similar to fevers caused by endotoxin and other inflammatory stimuli. Rats repeatedly injected with endotoxin develop tolerance to the fever-inducing action of endotoxin. We hypothesized that repeated pretreatment with endotoxin would modify the fever caused by exposure to psychological stress. To test this hypothesis, we compared open field-induced fevers in rats made endotoxin tolerant to those rats not endotoxin tolerant. We found that endotoxin tolerance had no effect on open field fevers.

Animals↗
PubMed1984

The assay of endotoxin by intravenous injection of lead acetate-treated mice.

A new intravenous endotoxin assay method (i.v. method) for the determination of very small amounts of endotoxin was studied in mice pre-treated intraperitoneally with lead acetate and was compared with an earlier intraperitoneal (i.p.) method in which both endotoxin and lead acetate were administered by the i.p. route. Linear dose-response relationships were obtained for both the i.v. and i.p. methods between logarithmic doses of endotoxin and the responses measured as body weight ratios on the first day. The range of the linearity was longer in the i.v. method than that in the i.p. method. In the i.v. method, linearity extended to much smaller doses of endotoxin than in the i.p. method. The slope of the dose-response line obtained by the i.v. method was flatter than that obtained by the i.p. method. The minimum detectable dose defined as the smallest dose of endotoxin producing a mean response statistically distinguishable from that of the control was in the nanogram order and smaller than that obtained by the i.p. method. Therefore the i.v. method may be more suitable than the i.p. method for detection of very small amounts of endotoxin. The non-parallelism of the dose-response lines obtained in lead acetate-treated and untreated mice was demonstrated in the i.v. method as well as in the i.p. method.

Animals↗
PubMed1999

Endotoxin and immune activation in chronic heart failure: a prospective cohort study.

BACKGROUND: Immune activation in patients with chronic heart failure may be secondary to endotoxin (lipopolysaccharide) action. We investigated the hypothesis that altered gut permeability with bacterial translocation and endotoxaemia would be increased in patients with oedema secondary to congestive heart failure. METHODS: We compared 20 patients who had chronic heart failure with recent-onset peripheral oedema (mean age 64 years [SD 10], New York Heart Association [NYHA] class 3.3 [0.7]), 20 stable non-oedematous patients with chronic heart failure (mean age 63 years [19], NYHA class 2.6 [0.7]), and 14 healthy volunteers (mean age 55 years [16]). Biochemical markers of endotoxaemia, inflammation, and immune activation were measured. Ten patients were studied within 1 week of complete resolution of oedema. Five patients survived longer than 6 months and were restudied again after remaining free of oedema for more than 3 months. FINDINGS: Mean endotoxin concentrations were higher in oedematous patients with chronic heart failure than in stable patients with chronic heart failure (0.74 [SD 0.45] vs 0.37 EU/mL [0.23], p=0.0009) and controls (0.46 EU/mL [0.21], p=0.02). Oedematous patients had the highest concentrations of several cytokines. After short-term diuretic treatment, endotoxin concentrations decreased from 0.84 EU/mL [0.49] to 0.45 EU/mL [0.21], p<0.05) but cytokines remained raised. After freedom of oedema for more than 3 months after oedema resolved, endotoxin concentrations remained unchanged from the previous visit (0.49 EU/mL [0.06], p=0.45). INTERPRETATION: Raised concentrations of endotoxin and cytokines are found in patients with chronic heart failure during acute oedematous exacerbation. Intensified diuretic treatment can normalise endotoxin concentrations. Our preliminary findings suggest that endotoxin may trigger immune activation in patients with chronic heart failure during oedematous episodes.

Acute-Phase Proteins↗
PubMed1998

Stress enhanced reduction in peripheral blood lymphocyte numbers in dairy cows during endotoxin-induced mastitis.

Two groups of Holstein dairy cows, which showed either high- (HC; n = 8) or low (LC; n = 10) plasma cortisol concentrations in response to a psychological stressor (novel-environment test) in their first lactation, were used 1 year later for studying the effects of psychological stress on various aspects of the host defence during endotoxin-induced mastitis. Social isolation was used as a stressor; endotoxin was used to activate the host defence. HC-cows appeared to be more stressed by the experimental procedure than LC-cows. One hour after having been isolated, rectal temperature increased (+0.59 degrees C) in HC- but not in LC-cows. Handling, related to the intra-mammary administration of endotoxin, induced a higher increase in cortisol concentration in HC- than in LC-cows 1 h after injection. In addition, HC-cows vocalised significantly more frequently (595 +/- 222) than LC-cows (81 +/- 24) between 1.5 and 9.5 h after isolation. Between 3 and 5.5 h after endotoxin-treatment, cortisol concentrations increased profoundly in both LC- and HC-cows and peaked at 24.6 +/- 3.8 and 22.8 +/- 3.1 ng ml(-1), respectively. The rise in plasma cortisol concentration was associated with a decrease in the number of circulating lymphocytes between 0 and 8 h post injection (PI). Between 8 and 10 h PI, the number of circulating lymphocytes in HC-cows further decreased (40%) to 1.58x10(6) cells ml(-1) and remained so until 21 h PI. This was not the case with the LC-cows. The results show that a differing sensitivity of dairy cows to environmental stressors is associated with a significant difference in the number of circulating leukocytes following intra-mammary administration of endotoxin during a period of social isolation. The results further suggest that, apart from adrenocortical hormones, other factors related to general stress-responsiveness modulate the number of peripheral lymphocytes in dairy cows during endotoxin-induced mastitis. During environmental stress, these factors may enhance endotoxin-induced reduction in circulating lymphocyte numbers, particularly in cows that are sensitive to environmental stressors. As to the clinical relevance of these differences in stress responsiveness, no differences between LC- and HC-cows were found in disease incidence nor in duration of a disease episode during both the 1st and 2nd lactation. In the 2nd lactation. HC-cows tended to produce less milk than LC-cows.

Animals↗
PubMed1985

Synergistic effect of liposomes and endotoxins on the activation of rat macrophage tumoricidal activity.

Macrophage biological responses to endotoxins have been extensively studied; nevertheless, the mechanisms by which endotoxins activate macrophage tumoricidal activity are not currently understood. We used liposomes to investigate the interaction of endotoxins with macrophages. In a medium containing 10 micrograms endotoxin/ml, macrophage-mediated cytolysis ranged from -7 to 36%. In all the experiments, 1mM dipalmitoyl phosphatidyl choline (DPPC) small unilamellar liposomes significantly induced or enhanced cytolysis, ranging from 30-90%. Liposomes and endotoxins had a synergistic effect on the macrophage cytolytic activity. This effect was dose-dependent on liposome concentration, ranging from 0.25-1 mM or 2 mM. Liposomes decreased the endotoxin concentration threshold necessary to induce cytolysis. They did not modify the kinetics of macrophage activation. Liposomes did not modify the binding of tumor cells to macrophages. The optimum synergistic effect was obtained when liposomes were present during the first 18 h of the mixed culture of macrophages and target cells, before adding endotoxins for the next 18 h. When cholesterol was added to DPPC (M/M), liposomes did not enhance but rather inhibited macrophage activation by endotoxins.

Animals↗
PubMed1992

Chronic and intradialytic effects of high-flux hemodialysis on tumor necrosis factor-alpha production: relationship to endotoxins.

Tumor necrosis factor-alpha (TNF alpha) likely plays a role in hemodialysis-associated complications. As TNF alpha is mainly produced by monocytes in response to endotoxins, we studied its production and the presence of circulating endotoxins in patients dialyzed on polyacrylonitrile (PAN) membrane. Spontaneous production of TNF alpha was observed in patients before the dialysis session and increased during the session. Endotoxins were present in serum from patients chronically dialyzed with PAN and increased during hemodialysis session. In addition, intradialytic decrease in CD14 antigen expression on circulating monocytes, which could be caused by endotoxins, was found. The continuous presence of low amounts of circulating endotoxins between sessions may explain the chronic increase in TNF alpha secretion, while high amounts of circulating endotoxins may account for intradialytic oversecretion of TNF alpha and downmodulation of CD14. We suggest that endotoxin-free dialysates should be a prerequisite for the use of high-flux membranes.

Acrylic Resins↗
PubMed2000

Systemic and local airways inflammatory response to endotoxin.

Endotoxin can be detected in house dust. Numerous studies have revealed that endotoxin exposure is a risk factor in increasing airway obstructive manifestations, both in occupational and domestic environments. In humans, inhalation of pure endotoxin induces systemic symptoms and a change in bronchial non-specific responsiveness, related with changes in blood and sputum inflammatory markers. However, some recent work suggests that, prior to airway disease development, endotoxin may have an atopy-protective effect. In particular, indoor endotoxin exposure in early life may protect against allergen sensitisation by enhancing type-1 immunity. Finally, since large variations between human immune responses to endotoxin have been reported, genetic mutations could alter the mechanisms of endotoxin recognition and contribute to the risk of atopy.

Allergens↗