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PubMed1956

Elevation of properdin levels in mice following administration of bacterial lipopolysaccharides.

The administration of a single small dose of bacterial lipopolysaccharide produces in mice a considerable rise in properdin levels. This is accompanied by an early, transient, non-specific increase in resistance to certain bacterial infections. Bacterial lipopolysaccharides were shown to possess far greater activity than other substances previously studied in bringing about an elevation of properdin levels. After the injection of bacterial lipopolysaccharides, high molecular weight substances appear in the circulation, which interfere with the combination of properdin with zymosan and thus affect the assay of properdin. The administration of small amounts of bacterial lipopolysaccharides to mice at appropriate times before experimental infection "conditions" the mice so that they maintain normal or elevated properdin titers during the infectious process in contrast to control mice which show a progressive decline in properdin to low levels and death. The significance of this observation and its relationship to natural resistance to Gram-negative pathogens are considered.

Animals↗

PubMed1986

Susceptibility of phenotypic variants of Haemophilus influenzae type b to serum bactericidal activity: relation to surface lipopolysaccharide.

After three serial passages of Haemophilus influenzae type b strain Fuju in rats, we recovered a variant, which differed in colonial morphology, serum sensitivity, and lipopolysaccharide configuration from the parent strain. The parent organism (Fuju) appeared iridescent and transparent on Levinthal agar, and the rat-passaged variant (rat3 Fuju) appeared iridescent and opaque. The transparent, parent strain Fuju was sensitive to the complement-mediated bactericidal activity of normal rat serum, and the opaque, rat-passaged strain rat3 Fuju was serum resistant. Serum killing of the serum-sensitive strain appeared to be mediated by the classic complement pathway. Both serum-resistant and serum-sensitive strains were killed equally well by immune rat and human serum. These two strains did not differ in the amount of capsular polysaccharide that they elaborated nor in their major outer membrane protein patterns on SDS-PAGE. Lipopolysaccharide isolated from these two strains demonstrated different electrophoretic mobility patterns. Furthermore, the organisms showed different reactivities with two monoclonal antibodies directed against determinants of Hib lipopolysaccharide. Thus, the difference in susceptibility to complement-mediated bactericidal activity of normal rat serum displayed by these two strains is associated with their phenotypes, appears to be unrelated to differences in major outer membrane proteins or in the amounts of capsular polysaccharide elaborated, and is associated with differences in surface lipopolysaccharides.

Animals↗

PubMed2002

Innate immune recognition of lipopolysaccharide by endothelial cells.

OBJECTIVE: The endothelium is an active component of the innate immune response to bacterial invasion. Endothelial cells comprise mechanisms to recognize structural patterns expressed by pathogens and subsequently initiate the transcription of inflammatory genes. The purpose of this article is to summarize the molecular processes that underlie the endothelial innate immune response to microbial components, with a particular focus on responses to Gram-negative bacterial lipopolysaccharide. DATA SOURCES: Personal observations and review of the literature as revealed by the National Library of Medicine. DATA SUMMARY AND CONCLUSION: Endothelial cells recognize the presence of microbial components such as lipopolysaccharide via a receptor complex that contains at least three important cell surface components: CD14, Toll-like receptor-4, and MD-2. CD14 and MD-2 exist as soluble receptor components and are thought to bind to both lipopolysaccharide and Toll-like receptor-4, whereas Toll-like receptor-4 itself is the transmembrane signal transducer. Single-point mutations in MD-2 or the cytoplasmic portion of Toll-like receptor-4 abrogate the response to lipopolysaccharide. The composition of this receptor and the recruitment and activation of various cytoplasmic proteins afford at least five levels of ligand specificity and suggest that there are at least as many potential therapeutic targets for Toll-like receptor-mediated inflammatory states, including sepsis.

Antigens, Surface↗

PubMed2002

Differential effects of lowering culture temperature on mediator release from lipopolysaccharide-stimulated neonatal rat microglia.

OBJECTIVE: Therapeutic moderate hypothermia has the potential for neuronal protection against brain injury. Microglia, a type of immune-related cell in the brain, may play a certain role in neuronal damage subsequent to injury. We examined the effects of culture temperature changes from 37 degrees C to 33 degrees C or 30 degrees C on mediator release, including nitric oxide, interleukin-6, and tumor necrosis factor-alpha from lipopolysaccharide-stimulated microglia harvested from neonatal rats. DESIGN: Laboratory study. SETTING: University medical school. SUBJECTS: Microglial cells isolated from primary cultures of rat brains. INTERVENTIONS: The production of nitric oxide was measured by a nitrite accumulation method in a culture medium, whereas cytokines, interleukin-6, and tumor necrosis factor-alpha were measured by enzyme-linked immunosorbent assay. MEASUREMENT AND MAIN RESULTS: At 30 degrees C and 33 degrees C, nitric oxide production stimulated by lipopolysaccharide decreased to 10 and 30% of control (37 degrees C), respectively, 24 hrs after the stimulation, and the decrease was sustained for 48 hrs. Interleukin-6 production at 30 degrees C and 33 degrees C was also reduced to 30% of control 6 hrs after the activation. Such responses lasted throughout the study. However, tumor necrosis factor-alpha release at 30 degrees C and 33 degrees C was depressed for only 6 hrs after stimulation, followed by subsequent elevation to concentrations similar to those at 37 degrees C. Microglial morphologic activation, showing changes from round to bipolar, reached a peak at 6 hrs in the 37 degrees C group, returning to round 12 hrs after lipopolysaccharide application. In 30 degrees C and 33 degrees C, the zenith was detected at 6 hrs, with activation remaining even 12 hrs after the stimulation, suggesting prolongation of the microglial response to lipopolysaccharide, which was inconsistent with changes in tumor necrosis factor release. CONCLUSIONS: Decreasing culture temperature inhibits the production of nitric oxide and interleukin-6 from activated microglia. Differences were found in the degree or time course change between tumor necrosis factor-alpha and the other mediators. Also, the time course of morphologic changes in microglia was dependent on culture temperature. Further studies are required to define the mechanisms for such differences in mediator release from cooled microglia and also to clarify the inconsistency between morphologic change and its function in the cell.

Animals↗

PubMed2006

Lipopolysaccharide found in aseptic loosening of patients with inflammatory arthritis.

Aseptic loosening of orthopaedic implants occurs in the absence of clinical signs of infection. Nevertheless, bacterial endotoxins derived from subclinical infections, systemic sources, or the implant manufacturing process may contribute to aseptic loosening. Also, the rate of implant infection is greater in patients with inflammatory arthritis than in patients with osteoarthritis. We hypothesized that lipopolysaccharide, the classic endotoxin derived from gram-negative bacteria, is more prevalent in periprosthetic tissue surrounding aseptically loose implants in patients with inflammatory arthritis than in patients with osteoarthritis. To test this, we used a modified Limulus amebocyte assay not affected by beta-glucan-like molecules in mammalian tissues. Lipopolysaccharide rarely was detected in periprosthetic tissue from patients with osteoarthritis and aseptic loosening (one of six patients). In contrast, lipopolysaccharide was detected despite the absence of any clinical signs of infection in peri-prosthetic tissue from all four patients with inflammatory arthritis (rheumatoid arthritis, juvenile rheumatoid arthritis, and systemic lupus erythematosus). Lipopolysaccharide also was detected in two patients with gram-negative infections, who were included as positive control subjects. Endotoxins derived from low-grade or systemic bacteremia may be important contributors to aseptic loosening particularly in patients with autoimmune conditions such as inflammatory arthritis.

Adult↗

PubMed2006

Insulin reduces the multiple organ injury and dysfunction caused by coadministration of lipopolysaccharide and peptidoglycan independently of blood glucose: role of glycogen synthase kinase-3beta inhibition.

OBJECTIVE: Insulin reduces morbidity and mortality among critically ill patients, but the molecular mechanisms of its effect remain unknown. Insulin is a well-known inhibitor of glycogen synthase kinase-3, which may play an important role in systemic inflammation and shock. Here we investigate the role of blood glucose and glycogen synthase kinase-3beta inhibition in the protective effect of insulin on the organ injury/dysfunction associated with excessive systemic inflammation. DESIGN: Prospective, randomized study. SETTING: University-based research laboratory. SUBJECTS: Eighty-five anesthetized Wistar rats. INTERVENTIONS: Rats received Escherichia coli lipopolysaccharide (1 mg/kg) and Staphylococcus aureus peptidoglycan (0.3 mg/kg) or vehicle intravenously. Insulin (1.4 units/kg intravenously) was administered in the absence or presence of continuous glucose administration (4.5 mg/kg/hr intravenously) either prophylactically or therapeutically. The potent and selective glycogen synthase kinase-3beta inhibitor TDZD-8 (1 mg/kg intravenously) or vehicle (10% dimethyl sulfoxide) was administered either prophylactically or therapeutically. MEASUREMENTS AND MAIN RESULTS: Coadministration of lipopolysaccharide and peptidoglycan resulted in increases in the serum levels of creatinine (indicator of renal dysfunction), alanine aminotransferase, and aspartate aminotransferase (indicators of liver injury) at 6 hrs. Insulin or TDZD-8 similarly attenuated the organ injury/dysfunction caused by lipopolysaccharide and peptidoglycan when given either prophylactically or therapeutically. Continuous glucose administration had no effect on blood glucose levels or organ injury/dysfunction at 6 hrs. Treatment with insulin or TDZD-8 reduced the plasma levels of the proinflammatory cytokine interleukin-1beta. In vitro, insulin or TDZD-8 caused similar reductions in the nuclear factor-kappaB p65 activity and similar increases in the phosphorylation of Ser9 of glycogen synthase kinase-3beta. CONCLUSIONS: Therapy with insulin or the potent and selective glycogen synthase kinase-3beta inhibitor TDZD-8 reduced the organ injury/dysfunction caused by lipopolysaccharide and peptidoglycan in the rat. We propose that the inhibitory effect of insulin on the activity of glycogen synthase kinase-3beta contributes to the protective effect of insulin against the organ injury/dysfunction caused by excessive systemic inflammation independently of any effects on blood glucose.

Analysis of Variance↗

PubMed2003

Delayed cerebrovascular protective effect of lipopolysaccharide in parallel to brain ischemic tolerance.

Cerebrovascular abnormalities, in endothelium and smooth muscle compartments, occur in the course of cerebral ischemia-reperfusion as evidenced by the impairment of endothelium-dependent relaxation and decrease in potassium inward rectifier density in occluded middle cerebral arteries (MCAs). The authors investigated whether a delayed vascular protection occurred in a model of brain ischemic tolerance. A low dose of lipopolysaccharide (0.3 mg/kg) administered 72 h before MCA occlusion induced a significant decrease in infarct volume. In parallel to this delayed neuroprotective effect, lipopolysaccharide prevented the ischemia-reperfusion-induced impairment of endothelium relaxation. In addition, lipopolysaccharide prevented the postischemic alteration of potassium inward rectifier-dependent smooth muscle relaxation as well as the decrease in potassium inward rectifier density measured by patch-clamp in dissociated vascular smooth muscle cells originated from the occluded MCA. These results suggest that during brain ischemic tolerance, lipopolysaccharide is able to induce both a delayed neuroprotective and vasculoprotective effect.

Animals↗

PubMed1975

Studies on lipopolysaccharides isolated from strains of Neisseria gonorrhoeae.

Lipopolysaccharides, extracted by phenol-water from five strains fo Neisseria gonorrhoeae, were purified by treatment with ribonuclease followed by multiple washes. These preparations were fatal to mice when administered in submicrogram amounts with actinomycin D, the LD50 values varying from 4 to 16 mug/kg. Analyses showed that all preparations contained glucose, galactose, glucosamine, heptose, 2-keto-3-deoxyoctonic acid and phosphate. All the lipopolysaccharides contained the same fatty acids, namely beta-OH-10:0, beta-OH-12:0, beta-OH-14:0, 12:0, 14:0,16:0, 16:1, 18:0 and 18:1. We were unable to detect significant differences between the lipopolysaccharides of virulent and avirulent gonococci or between penicillin-sensitive and resistant strains. Gonococcal lipopolysaccharides appeared to lack O-antigen side chains.

Animals↗

PubMed2005

Lipopolysaccharide stabilizes the crystal packing of the ABC transporter MsbA.

The ABC transporter MsbA is an integral membrane protein involved in the transport of lipid A and lipopolysaccharides to the outer leaflet of the inner membrane in bacteria. Here, the critical role of the natural substrate lipopolysaccharide in the crystallization and diffraction quality of MsbA crystals is reported. Initial crystals grown in complex with ATP-vanadate alone diffracted to approximately 9 A. Screening of the natural substrate lipopolysaccharides led to the crystallization of MsbA in complex with ADP-vanadate and Ra lipopolysaccharide. The increased order within the crystal lattice allowed structure determination to 4.2 A.

ATP-Binding Cassette Transporters↗

PubMed2004

Induction of calprotectin release by Porphyromonas gingivalis lipopolysaccharide in human neutrophils.

Calprotectin, a major cytosolic protein of leukocytes, is detected in neutrophils, monocytes/macrophages, and epithelial cells. This protein is known to be a marker for several inflammatory diseases and is detected in inflammatory gingival tissue with periodontal disease. Recently, we found that the calprotectin level in gingival crevicular fluid from periodontitis patients was significantly higher than that of healthy subjects. However, the regulation of calprotectin in periodontal disease is unclear. In the present study, we investigated the effect of lipopolysaccharides of periodontopathic bacteria on calprotectin release from human neutrophils. Neutrophils from healthy donors were treated with lipopolysaccharides from Porphyromonas gingivalis (P-LPS), Actinobacillus actinomycetemcomitans, Prevotella intermedia, Fusobacterium nucleatum, and Escherichia coli. Calprotectin of neutrophil was identified by immunoblotting and calprotectin amount was determined by ELISA. Two subunits (10 and 14 kDa) of calprotectin were observed in the cell and medium fractions from neutrophils. P-LPS increased calprotectin release from seven to 16 times the control level after 30 min and its effect appeared in a dose-dependent manner (10-1000 ng/ml). Lipopolysaccharides from A. actinomycetemcomitans, P. intermedia, F. nucleatum, and E. coli also induced calprotectin release from neutrophils. These results suggest that lipopolysaccharides from periodontopathic bacteria induce calprotectin release from human neutrophils.

Adult↗

PubMed1982

The protein-lipopolysaccharide complex extracted with trichloracetic acid from Salmonella typhimurium effective in protection of mice against S. typhimurium infection.

A protein-lipopolysaccharide complex has previously been postulated as necessary to protect susceptible mice against Salmonella typhimurium infection. Lipopolysaccharide attached to non-specific proteins, bovine serum albumin or methylated BSA, gave a specific delayed-type hypersensitivity (DTH) reaction when injected into the footpad of mice sensitized with sublethal doses of S. typhimurium. However, immunization of BALB/c mice with the complex gave no survivors after challenge with 100 LD50 S. typhimurium. Trichloracetic acid extraction of bacterial cultures produced lipopolysaccharide with attached protein. This method gave simple and convenient production of an active factor, demonstrating few major protein bands after electrophoresis. The complex elicited specific DTH reactions in sensitized mice and protected 37% of BALB/c mice against 100 LD50 S. typhimurium. Combinations of protein:lipopolysaccharide were used in DTH experiments to determine the relative importance of the components. A minimum requirement for both was demonstrated, although the ratio was not critical. Use of O-antigenic mutant strains of Salmonella indicated a role for protein in the specificity of activity of the complex.

Animals↗

PubMed1994

Analysis of Oct2-isoform expression in lipopolysaccharide-stimulated B lymphocytes.

Oct2-isoform expression in splenic B cells stimulated with lipopolysaccharide or lipopolysaccharide plus phorbol-di-butyrate was analysed by cDNA cloning. The frequency of Oct2-positive clones was 1/15,000 in both libraries. Two new isoforms were found that generate novel amino- or carboxy-terminal sequences. An isoform lacking exon 11 destroyed the carboxy-terminal leucin-zipper region and introduced a frame shift creating a novel, proline-rich carboxy terminus. A new exon containing a highly basic region (4c) was characterized, between exons 4 and 5. This exon was inserted between glutamine-rich regions 2 and 3, carboxy terminal of a tentative leucine-zipper structure. In addition, a new combination isoform containing Oct2a's amino terminal insert (exon 7a) and Oct2b's carboxy terminal insert (exon 13) was found that created a novel large isoform, Oct2ab. More frequent use of the classical Oct2a and Oct2b isoforms was observed in the lipopolysaccharide-stimulated B cells, while a preference for the Oct2ab and Oct2ba isoforms was observed in lipopolysaccharide plus phorbol-di-butyrate-treated cells.

Amino Acid Sequence↗

PubMed1975

Electrodialysis of lipopolysaccharides and their conversion to uniform salt forms.

Ions of low molecular weight like metal cations and basic amines are present in lipopolysaccharides regardless of the isolation procedure employed. They are present in salt form with the acidic groups of the molecule and, partly, bound by chelation. Electrodialysis which removed a large proportion of these basic materials led to acidic lipopolysaccharides often with reduced solubility. Electrodialyzed lopopolysaccharides could be rendered soluble by neutralizing with alkali or with a basic amine. Depending on the base employed for neutralization preparations were obtained which showed in water distinct differences in solubility, viscosity and opalescence. These differences were related to differences in the sedimentation coefficients of the various salt forms. Neutralization with triethylamine led in all cases to highly soluble preparations with low sedimentation coefficients, while, on the other hand, neutralization with Mg(OH)2 led in most cases to insoluble preparations. The acidic lipopolysaccharides obtained by electrodialysis deteriorate on storing in a freeze-dried form. On heating in distilled water autohydrolysis occurs and free lipid A is liberated. The lipid A which is so far known as a water-insoluble material showed increased solubility when prepared from electrodialyzed lipopolysaccharides.

Dialysis↗

PubMed1976

Cell-wall lipopolysaccharides of ampicillin-resistant mutants of Escherichia coli K-12.

The lipopolysaccharides of ampicillin-resistant cell-wall-defective mutants of Escherichia coli K-12 were analyzed. From their lipopolysaccharides the respective core oligosaccharides were obtained. Following dephosphorylation,the core oligosaccharides were methylated and analyzed by gas chromatography/mass spectrometry. From core-defective mutants substructures of the K-12 core were obtained. Analysis of the lipopolysaccharide preparations from wild-type K-12 indicated the presence of several core structures with different degrees of completion. The lipopolysaccharide preparation was degraded and the oligosaccharide mixture was partially resolved by gel filtration chromatography. Methylation, gas chromatography and mass spectrometry of the oligosaccharides permitted the tentative formulation of the K-12 core structure. Alternative interpretations for this heterogeneity are discussed.

Ampicillin↗

PubMed1976

Phospholipid and lipopolysaccharide in Proteus mirabilis and its stable protoplast L-form. Difference in content and fatty acid composition.

Cells of the stable protoplast L-form of Proteus mirabilis contain 1.5 to 2 times more extractable lipid, mostly phospholipid, per dry weight than cells of the bacterial form. Under identical conditions of cultivation the qualitative and quantitiative composition of the phospholipid is very similar in both cell forms. The range of mole percentages of individual phospholipid species is 78-80 for phosphatidylethanolamine, 10-13 for phosphatidylglycerol, 3.9-5.5 for diphosphatidylglycerol and 1.0-2.1 for lysophospholipid. However, all phospholipid species in the L-form differ from those of the bacterial form by a lower content of long-chain fatty acids and a higher content of short-chain fatty acids. Growth of the L-form in the presence of growth-stimulating horse serum results in a change of phospholipid composition accompanied by the uptake of phospholipid and fatty acids from the serum into L-form phospholipid. L-form protoplasts synthesize the same two types of lipopolysaccharide, I and II, that were previously identified in the bacterial form of Proteus mirabilis. However, only small amounts of the more hydrophilic lipopolysaccharide II are present in the L-form. Lipopolysaccharides from both cell forms have virtually identical polysaccharide compositions but differ strikingly in the relative content of fatty acids in their lipid-A moieties. Molar ratios of tetradecanoic acid, hexadeconoic acid and 3-hydroxytetradecanoic acid are 5:1:6 in the bacterial form and 5:0:1:6 in the L-form grown in serum-free medium. The observated differences between the bacterial form and the protoplast L-form are interpreted as results of the adaptation of the L-form to life in the state lacking an envelope by formation of a physically more stable but still sufficiently fluid protoplast membrane. A rapid method based on fatty acid analysis for the simultaneous quantitative determination of phospholipid and lipopolysaccharide content of whole cells is reported.

Cell Division↗

PubMed1977

A 31P-nuclear-magnetic-resonance study of the phosphate groups in lipopolysaccharide and lipid A from Salmonella.

Untreated and partially deacylated lipopolysaccharides from various P- and P+ strains of Salmonella were studied with 31P nuclear magnetic resonance spectroscopy and by conventional analytical methods. The spectral signals were assigned to various phosphate groups in the lipid A moiety and in the oligosaccharide part. A signal at +2.3 ppm could be assigned to a phosphodiester linkage formed between 4-amino-4-deoxyl-L-arabinose linked via the glycosidic hydroxyl group to the 4'-phosphate group of the glucosamine disaccharide in the lipid A moiety. A strong pyrophosphate signal at +11 ppm in P- strains was identified as a pyrophosphoryl ethanolamine group at the glycosidic end of this glucosamine disaccharide unit. No evidence was found for phosphodiester or pyrophosphodiester bonds crosslinking lipopolysaccharide 'subunits'. A revised version of the lipid A structure of Salmonella is presented. By a combination of 31P nuclear magnetic resonance spectroscopy data and conventional analytical methods the extent to which the lipopolysaccharides are substituted by various phosphate groups on the lipid A and the oligosaccharide moiety could be estimated. It was thus shown that substantial heterogeneity, leading to several molecular species of lipopolysaccharides is caused by addition or omission of certain groups. Since changes in substitution were found to be dependent on the growth conditions, it is thought possible that the overall negative surface charge of Salmonella can be modified by addition or omission of neutralising amino groups from ethanolamine and/or 4-amino-4-deoxy-L-arabinose, and can thus be adapted to the environment.

Carbohydrates↗

PubMed1978

N-Acetylneuraminic acid: a constituent of the lipopolysaccharide of Salmonella toucra.

The composition of lipopolysaccharide and polysaccharides isolated after acidic or alkaline degradation of lipopolysaccharide of Salmonella toucra has been investigated. The following analytical methods were used in this study: gel-filtration and ion-exchange techniques, paper and gas-liquid chromatography as well as spectrophotometric analysis. The products of the lipopolysaccharide degradation were fractionated on the Sephadex G-25 and Sephadex G-50 columns. Lipopolysaccharide and products of its degradation besides glucosamine, galactose, glucose, heptose(s) and 3-deoxy-D-manno-octulosonate described as 'basal' sugars, also contained N-acetylneuraminic acid and an unidentified amino sugar.

Carbohydrates↗

PubMed1986

Formation and metabolism of leukotriene C4 in macrophages exposed to bacterial lipopolysaccharide.

Lipopolysaccharide (10 micrograms/ml) was found to stimulate resident mouse peritoneal macrophages to produce leukotriene C4 (36 +/- 1.3 ng/10(6) cells, SEM, n = 20) within 16 h. Spontaneous synthesis in control cultures without lipopolysaccharide was less than 1.6 ng/10(6) cells. Leukotriene C4 was characterized by reversed-phase high-performance liquid chromatography, ultraviolet spectrometry and radioimmunoassay. When the macrophages, prelabeled with [3H]arachidonic acid, were treated with lipopolysaccharide radioactivity was incorporated into leukotriene C4. The amount produced varied with the method of macrophage preparation and incubation conditions and was dependent on the amount of lipopolysaccharide added (0.5-60 micrograms/ml), on cell counts and on the incubation time (4-16 h). The released leukotriene C4 was converted to a compound identified as a C6-cysteinylleukotriene, indicating metabolism of the leukotriene by the macrophages. Parallel determinations of prostaglandins E2 and F2 alpha by radioimmunoassay demonstrated that leukotriene C4 and prostaglandin E2 are formed by mouse peritoneal macrophages to a similar degree.

Animals↗