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PubMed1982

Different sugar compositions of lipopolysaccharides isolated from phase I and pure phase II cells of Coxiella burnetii.

The compositions of lipopolysaccharides I and II, isolated from Coxiella burnetii phase I and pure phase II cells, respectively, showed drastic and clear-cut differences. Lipopolysaccharide II exhibited a comparatively simple composition. It contained, in addition to glucosamine (from lipid A) and a 2-keto-3-deoxyoctulosonic acid-related, thiobarbituric acid-positive substance, only two aldoses in high amounts, namely D-mannose and D-glycero-D-mannoheptose. Lipopolysaccharide I contained the same components, but it also contained at least eight other constituents including neutral sugars, e.g., an unusual branched sugar (3-C-methyl-6-deoxy-hexose) and unusual aminohexoses. Some components were characterized by a very high retention time in gas-liquid chromatography. The similarity of the phase variation in C. burnetii to the well-known smooth-to-rough mutation found in Enterobacteriaceae is discussed. Cells of phase I correspond to enterobacterial smooth forms, whereas cells of phase II might be compared to the rough forms.

Amino Sugars↗

PubMed1984

Lipopolysaccharide, capsule, and fimbriae as virulence factors among O1, O7, O16, O18, or O75 and K1, K5, or K100 Escherichia coli.

K1, K5, and K100 Escherichia coli isolates of the lipopolysaccharide antigen types O1, O7, O16, O18, or O75, which had formerly been assigned to clonal groupings were compared with K? E. coli isolates and with laboratory-derived mutants defective in capsule or lipopolysaccharide synthesis. The amount of K1 capsule, the length distribution of the lipopolysaccharide, and the expression of type I and P fimbriae were determined. The clonal groupings were uniform with regard to these properties within each group but different from each other. Many of the K? strains differed from the clonal representatives. The results are interpreted with regard to the different diseases caused by each of these bacterial groups.

Cell Membrane↗

PubMed1984

Immunochemical characterization of rough Brucella lipopolysaccharides.

Lipopolysaccharides (LPS) were extracted from rough strains of Brucella abortus and Brucella melitensis and from strains of the naturally occurring rough species Brucella ovis and Brucella canis. Brucella rough lipopolysaccharides (R-LPS) were readily distinguished from Brucella smooth lipopolysaccharides (S-LPS) and enterobacterial R-LPS, by their chemical, physical, and serological characteristics. B. ovis R-LPS was differentiated from B. abortus, B. melitensis, and B. canis R-LPS by its reaction of partial identity in immunodiffusion. Monospecific mouse sera against B. ovis R-LPS agglutinated only the homologous bacteria but not R cells of other species of Brucella. B. ovis R-LPS contained more 2-keto, 3-deoxyoctonate, and glucosamine as a percentage of dry weight than any other R-LPS tested. B. abortus R-LPS was identified by the absence of an unidentified sugar present in the other R-LPS molecules, and B. melitensis R-LPS could be differentiated from B. canis R-LPS by its higher content of fatty acids. In contrast to S-LPS, all of the R-LPS studied lacked quinovosamine. In electron micrographs, Brucella R-LPS had a granular appearance, in contrast to typical lamellar structures formed by Brucella S-LPS and Escherichia coli R-LPS.

Animals↗

PubMed1984

Expression of lipopolysaccharide O antigen in Escherichia coli K-12 hybrids containing plasmid and chromosomal genes from Shigella dysenteriae 1.

The requirement for both plasmid and chromosomal genes in the biosynthesis of Shigella dysenteriae 1 lipopolysaccharide O antigen was demonstrated in Escherichia coli-Shigella hybrids. A 6-megadalton S. dysenteriae 1 plasmid, designated pWR23, was phenotypically tagged with the Tn3 ampicillin-resistance transposon. The tagged plasmid, designated pWR24, was transferred by transformation or conjugal mobilization to a rough E. coli K-12 recipient. Although the resultant hybrids were agglutinated in S. dysenteriae 1 antiserum, they did not remove all of the anti-Shiga agglutinins in absorption experiments. Modified lipid A core structure was detected in these hybrids, but Shiga O antigen was not expressed. When the his+ locus of the S. dysenteriae 1 chromosome was transferred by transduction to E. coli K-12 containing pWR24, complete Shiga O antigen was expressed. Lipopolysaccharide extracted from these hybrids was indistinguishable chemically, electrophoretically, and serologically from native S. dysenteriae 1 lipopolysaccharide.

Antigens, Bacterial↗

PubMed1985

Cyclic development of immunological memory to bacterial lipopolysaccharide.

Immunological memory to the lipopolysaccharide of Escherichia coli O113 was generated in strains of inbred mice given a single subimmunogenic dose of either E. coli O113 lipopolysaccharide or the native protoplasmic polysaccharide of E. coli O113. Such memory, which only involved antibody of the immunoglobulin M class, developed in a cyclic manner that was characteristic for the strain of mice used. It involved cell proliferation as well as differentiation and persisted for at least 25 days after priming with a single injection of a subimmunogenic dose of E. coli O113 lipopolysaccharide.

Animals↗

PubMed1985

Bacterial lipopolysaccharide induction of leukocyte-derived corticotropin and endorphins.

Previous reports have shown that there is an endogenous opioid component associated with pathophysiological responses to endotoxin. It has been shown that these responses are alleviated by naloxone, a specific opiate antagonist. Results of another study have indicated that leukocytes may mediate some of those responses since leukocyte depletion alleviated the effects of lipopolysaccharide. In view of the above reports as well as the finding that leukocytes produce immunoreactive (ir-) endorphins and corticotropin (ACTH) when stimulated with Newcastle disease virus or ACTH-releasing factor, we postulated that leukocytes may serve as an extrapituitary source of endorphins produced in response to bacterial endotoxin. To test this hypothesis, human peripheral blood leukocytes as well as mouse spleen cells were cultured in vitro with Escherichia coli lipopolysaccharide for 48 h. The lipopolysaccharide (i.e., endotoxin) was shown to induce de novo synthesis of ir-ACTH and ir-endorphins. The leukocyte-derived ir-ACTH had a molecular weight of approximately 2,900 and demonstrated a bioactivity similar to that of pituitary-derived ACTH. The lymphocyte-derived ir-endorphin comigrated with alpha- and gamma-endorphin at approximately 1,800 daltons and was shown to bind to brain opiate receptors. These findings imply that leukocyte-derived endorphins may be involved in the pathophysiological response to endotoxin.

Adrenocorticotropic Hormone↗

PubMed1992

Novel adjuvant action of lipopolysaccharides that possess mannose homopolysaccharides as O-specific polysaccharides on immune responses to nonimmunogenic autoantigens in mice.

The adjuvant action of various lipopolysaccharides on immune responses to syngeneic tissue extract in mice was examined. Only lipopolysaccharides possessing the linear mannose homopolysaccharides as O-specific polysaccharides exhibited definite adjuvant action on immune responses to the autoantigens. The intensity of this adjuvant activity of lipopolysaccharide from Klebsiella O3 seemed to be the strongest.

Animals↗

PubMed1992

Lipopolysaccharide-tumor necrosis factor-glucocorticoid interactions during cecal ligation and puncture-induced sepsis in mature versus senescent mice.

Previous work in our laboratory demonstrated increased sensitivity of senescent (24-month-old) mice to cecal ligation and puncture (CLP) sepsis compared with that of mature (12-month-old) mice. In this study the median lethal dose of the strain of Escherichia coli most frequently isolated during CLP sepsis was determined. No significant age-associated difference in the mean lethal dose or the mean survival time was noted; however, sham surgery before injection of E. coli decreased the mean lethal dose by at least 100-fold. With surgical manipulation, the average time to death after bacterial injection simulated more closely that observed after CLP surgery. Host responses to CLP sepsis were investigated by measuring the levels of corticosterone, glucose, and tumor necrosis factor (TNF) in the sera of mature and senescent mice at 2-h intervals after surgery. Corticosterone levels increased gradually during the course of sepsis in mature mice; however, senescent mice demonstrated a pronounced elevation in hormone levels at 2 and 4 h after surgery. At subsequent sampling intervals the corticosterone levels remained elevated, although they were similar for both ages. At all sampling intervals, the glucose levels in serum were lower in senescent mice than in mature mice. Pronounced hypoglycemia (less than 80 mg/dl) was observed in senescent mice at 8 h postsurgery. TNF was detected in serum within a narrow time frame in both age groups at 6, 8, and 10 h postsurgery. Although elevated TNF levels in serum were not seen in every mouse in each group (approximately 50%), the data hinted that senescent animals produced larger quantities of TNF during CLP sepsis than did mature animals. E. coli lipopolysaccharide (1 mg/kg) was injected intraperitoneally, and the TNF levels in serum and peritoneal lavage fluid were measured at 30, 60, and 90 min. Senescent mice demonstrated a level of TNF in serum at 90 min after lipopolysaccharide treatment that was 20-fold higher than that of mature mice (299,877 pg/ml versus 15,594 pg/ml). The amount of TNF produced locally in the peritoneum was also substantially higher in senescent mice than in mature animals (1,716 pg/ml versus 776 pg/ml). The increased production of TNF in senescent animals, despite elevated circulating corticosterone levels, suggested an age-related defect in glucocorticoid-directed downregulation of TNF production. This was confirmed in lipopolysaccharide-treated animals given exogenous dexamethasone.(ABSTRACT TRUNCATED AT 400 WORDS)

Aging↗

PubMed1993

Lipopolysaccharide and granulocyte colony-stimulating factor delay neutrophil apoptosis and ingestion by guinea pig macrophages.

In previous studies, neutrophil-ingesting macrophages were clearly and easily observed in the peritoneal cavity of guinea pigs after intraperitoneal injection of thioglycolate medium, and phagocytosis of neutrophils by macrophages could be detected in in vitro cultures of peritoneal exudate cells. Using an in vitro system, we examined the effect of bacterial lipopolysaccharide and recombinant human granulocyte colony-stimulating factor on the apoptosis (programmed cell death) of neutrophils and their subsequent ingestion by macrophages. Lipopolysaccharide delayed karyopyknosis and apoptosis of neutrophils, as shown by endogenous endonuclease activity and a high proportion of trypan blue-excluding cells, and subsequent ingestion by autologous macrophages. Granulocyte colony-stimulating factor also delayed neutrophil karyopyknosis and ingestion by macrophages. When a thioglycolate medium was coinjected intraperitoneally with lipopolysaccharide into guinea pigs in the in vivo system, delays in neutrophil disappearance and ingestion by macrophages in the peritoneal cavity were also observed. We suggest that bacterial products and cytokines regulate neutrophil apoptosis and subsequent ingestion by macrophages at inflamed sites.

Animals↗

PubMed1994

Bacterial endosymbiont-derived lipopolysaccharides and a protein on symbiosome membranes in newly infected amoebae and their roles in lysosome-symbiosome fusion.

Experimental results are presented to support the view that symbiont-derived lipopolysaccharides are involved in the prevention of lysosome-symbiosome fusion in xD amoebae harboring bacterial endosymbionts. Monoclonal antibodies against lipopolysaccharides and a 96-kDa protein present on symbiosome membranes of amoebae were used to monitor the appearance of the membrane-specific components in newly infected amoebae with endosymbionts from xD amoebae. The lipopolysaccharides and protein appeared on the newly forming symbiosome membranes within 3 to 7 days, as detected by indirect immunofluorescence staining with monoclonal antibodies. The lysosome-symbiosome fusion was followed by double staining of two antigens with different monoclonal antibodies applied to the same amoeba. Antilipopolysaccharide monoclonal antibodies were detected by staining with a fluorescein isothiocyanate-conjugated secondary antibody, and a biotinylated anti-lysosomal protein monoclonal antibody was detected by staining with Texas Red-conjugated streptavidin. In xD amoebae injected with an antilipopolysaccharide antibody, lysosomes fused with some of the symbiosomes that did not fuse with lysosomes in noninjected cells.

Amoeba↗

PubMed1994

Dimethyl sulfoxide modulates NF-kappa B and cytokine activation in lipopolysaccharide-treated murine macrophages.

Antioxidants are protective against septic shock in animal models. Recently, free radical scavengers have been found to inhibit the activation of the NF-kappa B protein in a number of cell lines. This transcriptional regulatory protein binds to the promoters of the proinflammatory cytokines tumor necrosis factor, interleukin-6, and the macrophage inflammatory proteins. The current work examined lipopolysaccharide-induced NF-kappa B activation in the J774 macrophage-like cell line and primary peritoneal macrophages from lipopolysaccharide-responsive (C3HeB/Fej) and -nonresponsive (C3H/HeJ) murine strains. The DNA-binding activity of the NF-kappa B protein directly correlated with mRNA expression for the genes encoding the proinflammatory cytokines and the free radical scavenging enzyme, superoxide dismutase. Both the p50 and p65 NF-kappa B subunits were detected on gel supershift assays. Minimal NF-kappa B activity was observed following exposure of C3H/HeJ macrophages to lipopolysaccharide. The antioxidant dimethyl sulfoxide decreased the level of NF-kappa B activation in the J774 cells. This correlated with decreased expression of cytokine mRNAs and tumor necrosis factor bioactivity. These results suggest that modulation of NF-kappa B activation may provide a mechanism through which antioxidants protect against endotoxemia in murine models.

Animals↗

PubMed1999

Vibrio anguillarum resistance to rainbow trout (Oncorhynchus mykiss) serum: role of O-antigen structure of lipopolysaccharide.

The sensitivity of Vibrio anguillarum to the bactericidal effect of rainbow trout serum was investigated with different strains of serogroups O1 and O2a, which are the most frequently found serogroups in clinical outbreaks of vibriosis. All of the V. anguillarum strains were able to activate complement in rainbow trout serum, but smooth strains of V. anguillarum serogroup O1 were resistant to complement-mediated killing in the absence of specific antibodies. In the case of V. anguillarum serogroup O2a strains, 80% of the analyzed strains were resistant to rainbow trout serum even when specific antibodies were present. Analysis of the lipopolysaccharide structures of the tested V. anguillarum strains showed a positive correlation between the O-antigen size of the lipopolysaccharide and resistance to serum killing. The classical complement pathway was responsible for the antibody-dependent serum killing of susceptible V. anguillarum strains. When serum-resistant V. anguillarum serogroup O2a strains were grown in glucose-enriched Lennox L broth, they produced lipopolysaccharide molecules with fewer high-molecular-weight O-antigen units than did strains grown in broth without the addition of glucose. Strains grown in glucose-enriched medium became sensitive to rainbow trout serum killing, indicating that the high-molecular-weight O-antigen side chains prevented the activated complement from damaging the bacterium.

Animals↗

PubMed1969

Biosynthesis of cell wall lipopolysaccharide in mutants of Salmonella. V. A mutant of Salmonella typhimurium defective in the synthesis of cytidine diphosphoabequose.

A mutant of Salmonella typhimurium LT2 was found to be unable to convert cytidine diphospho-4-keto-6-deoxy-d-glucose into cytidine diphosphoabequose. The mutation maps in the rfb gene cluster, which is known to be involved in the biosynthesis of the peripheral, "O side-chain" portion of cell wall lipopolysaccharide. In spite of the fact that, in the O side chains, abequose is not a part of the main chain but occurs as short branches, the mutant appears to be unable to polymerize oligosaccharide "repeat units" into long O side chains. The following evidence indicates that this failure is the result of the absence of cytidine diphosphoabequose rather than that of a superimposed second mutation in other genes of the rfb cluster. (i) The mutant does not behave like a multisite mutant in genetic crosses, and it gives rise, at a high frequency, to "revertants" where the ability to synthesize cytidine diphosphoabequose and the ability to synthesize normal lipopolysaccharide with O side chains are both restored. (ii) The mutant strain has normal levels of activity of all of the other enzymes known to be involved in O side-chain synthesis, except that the levels of several enzymes were lowered by about 30% owing to the polarity effect of the mutation. That the lowering of these enzymes is not responsible for the failure of the mutant to synthesize O side chains is clear from the fact that there were revertants which had regained some ability to synthesize abequose but still had lowered levels of these other enzymes, and that this type of revertant produced lipopolysaccharide with considerable amounts of O side chains.

Carbohydrates↗

PubMed1974

Protein composition of the outer membrane of Salmonella typhimurium: effect of lipopolysaccharide mutations.

The protein composition of the outer membrane of Salmonella typhimurium has been analyzed by electrophoresis on slabs of sodium dodecyl sulfate-acrylamide gel. This powerful technique allows very high resolution of protein mixtures and has permitted the identification of multiple major protein components of the outer membrane; no evidence for a single major component of molecular weight 44,000 was obtained. These proteins were shown to be decreased in amount in mutants which have defective lipopolysaccharides. Mutants of an apparently new type were also found which contain decreased amounts of the proteins and the parent-like lipopolysaccharide, yet are resistant to a lipopolysaccharide-specific phage, C21. Several outer membrane proteins are insoluble in sodium dodecyl sulfate unless heated at high temperature (above 70 C). A purification procedure based on this property is tentatively suggested.

Bacterial Proteins↗

PubMed1974

Degradative effect of phenol on endotoxin and lipopolysaccharide preparations from Serratia marcescens.

It has been established that the well-known deproteinizing action of hot 45% aqueous phenol on whole cells or isolated and purified endotoxin of Serratia marcescens 08 is caused by the cleavage of a phenol-sensitive linkage within the lipid moiety. As a result of this degradation, both the lipopolysaccharide and simple protein fragments retained a part of the lipid moiety. Although not proceeding at the same fast rate as the cleavage of the lipid moiety, such phenol treatment also caused a partial hydrolysis of the O-specific side chain and ester-bound fatty acids. Hydrolysis of the O-specific side chain accounted for 5% of the lipopolysaccharide and that of ester-bound fatty acids accounted for 11% of the total fatty acid content after 60 min of treatment. It is suggested that the presence of these degradation products is one of the main causes of the heterogeneity of endotoxin and lipopolysaccharide preparations.

Animals↗

PubMed1974

Participation of lipopolysaccharide genes in the determination of the enterobacterial common antigen: analysis of R mutants of Salmonella minnesota.

A series of R (rough) Salmonella minnesota mutants with rfb, rfe, and rfa mutations leading to various defects in the biosynthesis of cell wall lipopolysaccharide was analyzed as to their enterobacterial common antigen (CA) content. All mutants that had functional rfe genes were CA(+) as is the wild-type parent. This includes mutants with the most defective lipopolysaccharide core types, demonstrating that core structures are not a necessary part of CA. All rfe(-) mutants (complete lipopolysaccharide core, defective synthesis of O side chains) were defective in the synthesis of CA. A smooth strain was accidentally found to be CA(-); the mutation responsible for this defect was also located, like rfe, very close to ilv.

Antigens, Bacterial↗

PubMed1975

Membrane-associated nucleotide sugar reactions: influence of mutations affecting lipopolysaccharide on the first enzyme of O-antigen synthesis.

Both the synthesis of lipopolysaccharide O-antigen and the synthesis of peptidoglycan in Salmonella typhimurium proceed via membrane-bound glycosylated lipid intermediates. The first enzyme of each pathway transfers a sugar phosphate from a nucleotide sugar to the glycosyl carrier lipid (P-GCL). Each enzyme catalyzes an exchange reaction between the reaction product urine monophosphate, and the nucleotide sugar substrate. Several strains of S. typhimurium defective in lipopolysaccharide synthesis accumulate glycosylated lipid intermediates under appropriate conditions. In addition, strains lysogenic for phage P22 synthesize a glucose derivative of the carrier lipid. These strains were used to demonstrate the P/GCL requirement of the exchange reaction catalyzed by galactose-diphosphoglycosyl carrier lipid (GCL-PP-Gal) synthetase, the first enzyme of O-antigen synthesis. Enzyme activity is greatly reduced when glycosylated P-GCL accumulates on the cytoplasmic membrane. The exchange reaction catalyzed by the first enzyme of peptidoglycan synthesis is unaffected by the accumulation of O-antigen fragments on the carrier lipid and may interact with a different pool of P-GCL within the membrane. GCL-PP-Gal synthetase activity cannot be detected in the membranes of two rfa mutants that synthesize incomplete lipopolysaccharide core. Either the synthesis of GCL-PP-Gal synthetase or the stable integration of the enzyme into the membrane structure may be disrupted in the rfa mutants. Peptidoglycan synthesis is unaffected by the mutations affecting the core glycosyltransferases.

Antigens, Bacterial↗

PubMed1976

Distribution and composition of lipopolysaccharides from mycoplasmas.

Polymeric carbohydrates containing glycerol and fatty acids were isolated from whole cells and membranes of mycoplasmas by hot aqueous phenol extraction and gel filtration. Lipopolysaccharides were found to occur in four species of Acholeplasma, two of Anaeroplasma, and in Mycoplasma neurolyticum. None were detected in Spiroplasma citri or in five species of Mycoplasma. All lipopolysaccharides contained both neutral and N-acylated amino sugars in ratios varying from 1:1 to 3:1. The neutral sugars found in varying distribution were glucose, galactose, and mannose. The amino sugars included fucosamine, an unidentified deoxyhexosamine, galactosamine, and glucosamine. Fucosamine and glucose were the only sugars common to all lipopolysaccharides. The fatty acids were similar to those found in the lipids of each organism.

Acholeplasma↗