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At least 1,333 records · Page 74Linked to original sources
PubMed1994

LPS injected into the pregnant rat late in gestation does not induce fetal endotoxemia.

Endotoxin is abortifacient. Abortion may be due to maternal, fetal or combined endotoxemia. The present study was performed to evaluate if fetal rat endotoxemia was induced by maternal endotoxemia in late gestation. An intraperitoneal injection of smooth lipopolysaccharide (Escherichia coli LPS and Shigella flexneri LPS) or rough LPS (Rc mutant Escherichia coli LPS) induced Limulus activity in maternal plasma, but not fetal plasma. These results suggest that fetal rat endotoxemia is not induced during maternal endotoxemia. Thus, the abortion may not be due to fetal endotoxemia.

Animals↗
PubMed1976

[Effects of endotoxinemia on renal and intrarenal hemodynamics of rats with or without portacaval anastomosis].

Renal dysfunction in patients with cirrhosis of the liver is frequent especially in connection with endotoxaemia. Renal and intrarenal haemodynamics were investigated, therefore, in normal rats with or without portacaval anastomosis (PCA) by means of the cardiac output (CO) fractionation technique using microspheres. The intrarenal blood distribution was estimated after anatomical separation of renal cortex and medulla. In normal rats the total renal fraction of CO was 22.5 +/- 7.2%, and the renal medulla fraction 0.8 +/- 0.4% of CO. After a single injection of E. coli-endotoxin (1.5 mg/kg b.w.) the animals developed a high-cardiac-output state, the mean arterial pressure decreased from 110 +/- 15 mm Hg to 81 +/- 6 mm Hg. Renal fraction of CO was unaltered but the blood flow through the kidney was increased due to the high CO. The blood flow of the medulla increased five to tenfold of control values whereas renal cortical blood flow decreased. During the first eight hours after endotoxin administration the animals developed polyuria with a decrease of urine osmolality. Comparable systemic and renal haemodynamics were present in untreated PCA-rats, in which endotoxaemia was present spontaneously (Limulus Gelation Test). Additional endotoxin administration in these animals caused severe shock syndrome with a decrease in total renal perfusion and a further decrease in renal cortical blood flow. Endotoxin administration in normal rats caused minimal morphological alterations in the kidneys which were comparable with those found in PCA-rats. Endotoxin administration in PCA-rats however leads to severe damage of the kidney with fibrin deposits in the glomerula and acute tubular necroses. The haemodynamic, functional and morphological changes caused by endotoxin in the experiments are observed in principle in patients with cirrhosis of the liver too. This indicates that endotoxin should be taken into considerations concerning the pathogenesis of renal failure in patients with cirrhosis of the liver.

Animals↗
PubMed1994

[Endotoxinemia in rats in the course of ethanol-induced liver damage].

Endotoxin concentrations were measured in the portal, hepatic venous blood and abdominal aorta of six groups of rats in experimental alcoholic liver injury. Groups of animal consisted of 16 rats: I.: control group; II.: rats received one dose of E. coli 0127: B8-3 mg/kg intraperitoneally (i.p.), III.: rats received three doses of E. coli; IV.: rats intoxicated with 20% ethanol ad libitum (60 days); V.: rats intoxicated with one dose of endotoxin after 20% ethanol ingestion; VI.: animal intoxicated with 20% ethanol and three doses of E. coli 0127: B8. The highest levels of endotoxin (determined by Limulus Lysate test) were in portal venous blood--3.1 pg/ml in control group to 113.4 pg/ml in VI. group. The level of endotoxin in plasma hepatic venous blood was elevated from 0.0 pg/ml (I., II. groups) to 15.8 pg/ml (III.), 34.3 pg/ml (IV.), 49.7 pg/ml (V.) up to 75.1 pg/ml (VI.). Plasma endotoxin concentration in abdominal aorta was highest in group VI.--32.2 pg/ml. The percentage of excretion rate of endotoxin by liver function was measured on the basis of difference between plasma endotoxin levels in the prehepatic blood (portal vein) and posthepatic blood (hepatic vein). The highest activity of biochemical parameters indicating liver injury was observed in animals intoxicated with ethanol and endotoxin.

Animals↗
PubMed1994

[Changes in blood endotoxin levels after scald in rats].

We quantified the portal blood endotoxin level as well as the systemic blood endotoxin level after scald in rats. The results show that the portal blood endotoxin level is significantly higher than the systemic blood endotoxin level (P < 0.001) in control group. In scald group the portal blood endotoxin level shows double peaks (increase significantly at second hour, decrease to normal at sixth hour and increase significantly again at twelfth hour), but the systemic blood endotoxin level remained low (P > 0.05). The results indicate that there is some endotoxin in the portal blood in normal condition, but large amount of endotoxin escape into portal blood in normal condition, but large amount of endotoxin escape into portal blood from the intestine in early stage after scald, resulting in enterogenous endotoxemia. The origin of systemic endotoxemia is discussed in the present article.

Animals↗
PubMed1994

A novel granulocyte-derived peptide with lipopolysaccharide-neutralizing activity.

Rabbit CAP18 (cationic antimicrobial protein, 18 kDa) is a leukocyte protein identified and purified using as an assay its capacity to bind and inhibit various activities of LPS. Oligonucleotide probes designed from the putative N-terminal protein sequence were used to obtain the corresponding cDNA from a rabbit bone marrow cDNA library. Examination of the cDNA sequence revealed that the protein fragment of the putative N-terminus was actually a 37-amino-acid C-terminal fragment. This fragment, designated CAP18(106-142), inhibits many activities of LPS. In the present studies, synthetic CAP18(106-142) is shown to: 1) bind to erythrocytes coated with diverse strains of LPS; 2) inhibit LPS-induced release of cytokines (TNF, IL-1, IL-6) and nitric oxide from macrophages; 3) inhibit LPS-induced LAL coagulation and 4) protect mice from LPS lethality. CAP18(106-142) may have therapeutic utility for conditions associated with elevated concentrations of LPS.

Amino Acid Sequence↗
PubMed1993

Removal of limulus reactivity and cytokine-inducing capacity from bicarbonate dialysis fluids by ultrafiltration.

Bicarbonate-based dialysate solutions support the rapid growth of bacteria. The long-term (360-h) efficacy of ultrafiltration by two polysulphone ultrafilters in removing not only endotoxin but also the cytokine(IL-1, TNF)-inducing capacity was evaluated using an experimental circuit contaminated with Pseudomonas aeruginosa filtrates. One of the polysulphone ultrafilters was submitted to a standard sanitization procedure every 12 h (hypochlorite 1.2% solution for 5 min and rinsing for 20 min). Endotoxin was detected by the kinetic quantitative chromogenic limulus amoebocyte lysate (LAL) assay. Immunoreactive IL-1 and TNF were evaluated in the lysates of peripheral blood mononuclear cells containing 5 x 10(5) human monocytes. The results of the present studies show that although LAL-reactive bacterial products were significantly removed in post-ultrafilter samples, they remained detectable, albeit below the upper limit accepted by the present European pharmacopeias (< 0.125 EU/ml). The removal of cytokine-inducing capacity was time-dependent and correlated with time of use in the case of the sanitized ultrafilter. Beyond the time of use, two other factors emerged as possibly capable of reducing the efficacy of the ultrafilter in removing LAL-reactive bacterial components, namely the pressure and the cytokine-inducing activity in pre-ultrafilter samples. Preincubation with polymyxin B, an agent that irreversibly binds lipid A and blocks lipid A-induced biological activities, did not abrogate the cytokine-inducing capacity in all post-ultrafilter samples; this suggests that either low-molecular-weight endotoxin subunits or lipid A-unrelated components may be responsible for the residual biological activity in post-ultrafilter samples.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1994

Functional domains of recombinant bactericidal/permeability increasing protein (rBPI23).

The 23-kDa recombinant amino-terminal bactericidal/permeability increasing protein fragment (rBPI23) has all of the antibacterial and antiendotoxin properties of the holoprotein. In the current studies, we have identified multiple active domains within rBPI23 with chemical and proteolytic cleavage fragments and with synthetic overlapping peptides. We also demonstrate a novel, high affinity heparin binding property for rBPI23, in addition to its established bactericidal and lipopolysaccharide binding properties. Cleavage fragments and synthetic, overlapping peptides of rBPI23 were analyzed for inhibition of the lipopolysaccharide-induced Limulus amebocyte lysate reaction, for bactericidal activity, and for heparin binding. Three separate, active domains were identified in amino acid regions 17-45, 65-99, and 142-169. A single synthetic peptide (85-99) was bactericidal. These results indicate that rBPI23 is comprised of three separate functional domains which contribute to the high affinity interaction of rBPI23 with Gram-negative bacteria. The individual activity of each domain and the cooperative interaction among domains provide the basis for developing rBPI23 analogues with increased biologic efficacy.

Amino Acid Sequence↗
PubMed1994

Monomeric Re lipopolysaccharide from Escherichia coli is more active than the aggregated form in the Limulus amebocyte lysate assay and in inducing Egr-1 mRNA in murine peritoneal macrophages.

Using the equilibrium dialysis apparatus, an aqueous suspension of predominantly aggregated Re lipopolysaccharide (ReLPS) from Escherichia coli D31 m4 (99.9% at 82.5 microM) can be processed to yield a solution of monomeric ReLPS at a saturation concentration of 77 ng/ml (3.4 x 10(-8) M). We compared the in vitro biological activities of these two physically distinct types of ReLPS preparations in two select assays, reaction in the Limulus amebocyte lysate (LAL) assay and induction of Egr-1 mRNA in macrophages. These assays were chosen for their rapid response times and relatively short incubation periods. The monomeric ReLPS was 179- and 1000-fold more active than the aggregated ReLPS preparation in the LAL assay and induction of Egr-1 mRNA by thioglycollate-elicited murine peritoneal macrophages, respectively. These results clearly showed that the monomeric ReLPS is the more active form. The lower biological activities of the aggregated ReLPS preparation might be due to the presence of a small amount of monomeric ReLPS (0.01-0.6%) produced during its preparation and the incubation periods in the biological assays. Thus, aggregated ReLPS may be relatively inactive.

Animals↗
PubMed1993

[Endotoxemia in severely burned patients].

Plasma endotoxin was determined by modified synthetic chromogenic limulus amebocyte lysate assay in 35 severely burned patients (30% to 98% TBSA). The results showed that the level of circulating endotoxin markedly increased during the early stage after injury, with a peak value at the 3rd postburn days. The relationship between burn size and the endotoxin value was significant (P < 0.01); The incidence of endotoxemia in the 35 patients was 36.8% to 74.7%. The plasma endotoxin concentrations of 7 burned patients with multiple system organ failure (MSOF) raced from 0.512 to 1.127 EU/ml, significantly higher than those of 10 patients without MSOF (0.216-0.553 EU/ml) at 3, 14, 21 and 28 postburn days. Endotoxemia in severely burned patients commonly occurred and was closely related to the development of sepsis and MSOF after burn injury. Dynamic observation of the changes in circulating endotoxin concentration was valuable as a marker for predicting sepsis and MSOF in critically ill patients with burns.

Adolescent↗
PubMed1993

[Experimental studies on the symptom-complex mechanism of pi man zao shi of dachengqi decoction].

Experiments have shown that Dachengqi Decoction can inhibit the activity of G-germs which commonly grow in the intestinal tract, inactivate the endotoxin directly in vitro, reduce the amplitude of fever caused by endotoxin injected intravenously, promote the gastric secretion and gastric retaining in rats, and increase the level of glycogen in liver. It also has some other effects. All these actions contribute to the explanation on the efficacy of Dachengqi Decoction to purge off the internal heat.

Animals↗
PubMed1993

Antagonistic effects of lipopolysaccharide binding protein and bactericidal/permeability-increasing protein on lipopolysaccharide-induced cytokine release by mononuclear phagocytes. Competition for binding to lipopolysaccharide.

Serum proteins play an important role in LPS-induced cell activation. The LPS binding protein (LBP) enhances cellular responses to LPS, whereas the polymorphonuclear leukocyte product bactericidal/permeability-increasing protein (BPI) inhibits LPS-induced cell activation. In this study the influences of LBP and BPI, two proteins with opposite effects, but with considerable sequence homology, on LPS-induced mononuclear phagocytic cell cytokine release was studied. LBP was shown to enhance LPS-induced TNF-alpha, IL-6, and IL-8 release by mononuclear phagocytic cells, whereas BPI inhibited the release of these cytokines. Furthermore, the effects of LBP and BPI on LPS-induced cytokine release by mononuclear phagocytic cells were shown to be counteractive. BPI interfered with the enhancing effect of LBP on the LPS-induced cytokine release. At high LBP to BPI ratios, BPI could no longer inhibit LBP-induced enhancement. In accordance, increasing concentrations of BPI abrogated the LBP effect. Next, it was shown that LBP and BPI compete for binding to LPS by using an assay system that detects binding of free BPI to an anti-BPI mAb. LPS prevented binding of BPI to anti-BPI mAb, whereas preincubation of LPS with LBP prevented the LPS-induced inhibition. Also, it was observed that both BPI and LBP inhibited LPS activity in the chromogenic LAL assay. We conclude from this study that LBP and BPI have counteractive effects on LPS-induced mononuclear phagocytic cell cytokine release by competing for binding to LPS.

Acute-Phase Proteins↗