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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

High-molecular weight lipopolysaccharide (O antigen enriched fraction) from Klebsiella pneumoniae was determined to be the receptor for bacteriophage FC3-1. A methodology for the identification of the lipopolysaccharide component involved in FC3-1 bacteriophage reception was used that is suitable for other phages and host bacteria.
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PMID:A high molecular weight lipopolysaccharide specific bacteriophage for Klebsiella pneumoniae. 305 77

Isogenic non-encapsulated (K-) mutants (O1:K-) were obtained from several different Klebsiella pneumoniae O1:K1 serotype strains. By employing K. pneumoniae bacteriophages FC3-1, FC3-2, and bacteriophage phi 1, the bacterial surface receptors of which, are the O1-antigen of lipopolysaccharide and the K1 capsular polysaccharide (K1) respectively, the K1 polysaccharide was found to completely cover the O1 lipopolysaccharide molecules in each of the O1:K1 strains examined. Exposure of the O-antigen at the cell surface was only observed after growth in the presence of sub-minimum inhibitory concentrations of antibiotics. The implications of these findings for the design of vaccines for the prevention of Klebsiella infections is discussed.
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PMID:Surface exposure of the O-antigen in Klebsiella pneumoniae O1:K1 serotype strains. 307 Feb 59

Natural and synthetic immunomodulators that increase non-specific resistance to infection induce the production of interleukin-1 (IL-1) and tumor necrosis factor (TNF). Therefore, we investigated the effect of IL-1 and of TNF on the survival of lethally-infected mice. Mice were injected with 1 x 10(6) Klebsiella pneumoniae in the thigh muscle. When recombinant human IL-1 beta was given as a single i.p. injection 24 h before the infection, survival was increased. Using 80 ng IL-1 beta per mouse, survival compared to control animals was 80% versus 20% 48 h after the infection (p less than 0.001). No effect of IL-1 was observed when it was given 1/2 h before or 6 h after the infection. IL-1 alpha proved to be at least as potent as IL-1 beta. Numbers of bacteria cultured from the blood, thigh muscle, liver, spleen, and kidney were similar in IL-1-treated and control animals. Protection against death by IL-1 was also investigated in granulocytopenic mice with a Pseudomonas aeruginosa infection. Administration of the cyclooxygenase-inhibitor, ibuprofen, did not affect the beneficial effect of IL-1. In this model human recombinant TNF was at least tenfold less active than IL-1 beta. Pretreatment with IL-1 also had a significant effect on survival of mice that received a high dose of bacterial lipopolysaccharide.
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PMID:The effects of recombinant interleukin-1 and recombinant tumor necrosis factor on non-specific resistance to infection. 307 57

The immunoprotective activity of Klebsiella pneumoniae K2 cell surface preparations and purified capsular polysaccharide was tested in mice. The 50% protective dose (PD50), expressed as capsular polysaccharide content, was 2 ng for cell surface preparations and 50 ng for purified capsular polysaccharide. Both preparations lost their immunoprotective activity after alkali treatment. Immune sera were raised in rabbits immunized with cell surface preparations. The precipitating and hemagglutinating capacity of these antisera was tested against either purified capsular polysaccharide or alkali-treated capsular polysaccharide. No difference was observed between the reactivity of the antisera against each antigen. The protective activity of these sera was tested on mice in passive transfer experiments, before and after absorption with either purified capsular polysaccharide or alkali-treated capsular polysaccharide. The sera lost their protective activity after absorption with purified capsular polysaccharide and after absorption with alkali-treated capsular polysaccharide. These experiments show that the difference in immunoprotective activity of cell surface preparations, purified capsular polysaccharide, and alkali-treated capsular polysaccharide is not due to a difference in their antigenic determinants. Cell surface preparations and purified capsular polysaccharide were fractionated by gel filtration on Sepharose 4B and by ultracentrifugation on cesium chloride density gradients. Three forms of capsular polysaccharide have been characterized. (i) A form of capsular polysaccharide with a very high protective activity (PD50 = 2 ng) that copurified with protein and lipopolysaccharide and was characterized by a low coefficient of distribution (Kd = 0.20) and a low density (1.5 to 1.6 g/cm3). (ii) A form of capsular polysaccharide with an intermediate protective activity (PD50 = 50 ng), contamined by less than 3% protein and 1% lipopolysaccharide, with a Kd of 0.35, and a density of 1.7 to 1.8 g/cm3. (iii) A nonimmunoprotective capsular polysaccharide obtained after alkali treatment of either cell surface preparations or purified capsular polysaccharide. The Kd of these fractions varied from 0.20 to 0.90 and their density from 1.7 to 1.8 g/cm3.
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PMID:Immunogenic properties of Klebsiella pneumoniae type 2 capsular polysaccharide. 309 40

We examined the ability of sera drawn from rabbits made tolerant to lipopolysaccharide (LPS) from Escherichia coli O18 to inhibit heterologous LPS-induced gelation of Limulus lysate. Compared with a pool of pretolerant sera, a pool of tolerant sera from these rabbits neutralized 5.5-fold more LPS from Salmonella typhimurium, 4.9-fold more LPS from Pseudomonas aeruginosa, and 10.0-fold more LPS from Klebsiella pneumoniae. Because previous studies have found that LPS bound to lipoprotein is less toxic than unbound LPS, we also studied the binding of LPS lipoprotein fractions in the serum pools by using fractionation with a cesium chloride-equilibrium density gradient. Radiolabeled LPS from E. coli O113 bound much more rapidly to lipoprotein fractions in tolerant serum than in pretolerant serum (after 11 min of incubation, 66.1% vs. 16.5% binding, respectively).
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PMID:Neutralization and lipoprotein binding of lipopolysaccharides in tolerant rabbit serum. 309 36

Three immunoglobulin preparations for intravenous infusion were compared in vivo to determine their relative protective capacity against several gram-negative and gram-positive pathogens. Polyglobin N is a conventional IgG concentrate. Psomaglobin N is identical in formulation to Polyglobin N but is prepared from the plasma of donors who have naturally high levels of antibody to lipopolysaccharide antigens of Pseudomonas aeruginosa. IgGMA is a conventional IgG concentrate containing 12% IgG and 16% IgA. In a murine model of burn wound sepsis the three IgG preparations were similarly protective against three or ten strains of P. aeruginosa. Psomaglobin N and Polyglobin N were significantly (p less than or equal to 0.015) more protective than IgGMA against six of ten and three of ten strains of P. aeruginosa, respectively. In a murine model of Streptococcus pneumoniae type 3 pneumonia, the three Ig preparations were similarly protective. IgGMA was significantly more protective (p less than or equal to 0.025) than Psomaglobin N and Polyglobin N against Salmonella typhimurium in murine peritonitis. However, the mean protective dose (PD50) of the two later preparations was less than or equal to 20 mg/kg body weight. In models of peritonitis both Psomaglobin N and Polyglobin N were more protective than IgGMA (p less than or equal to 0.004) against Haemophilus influenzae b, Klebsiella pneumoniae, Serratia marcescens 06:H3 and group B Streptococcus types 1b and 1c. Psomaglobin N and ciprofloxacin were employed to treat established polymicrobial murine burn wound sepsis resulting from contamination of the burn site with mixtures of P. aeruginosa and Staphylococcus aureus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Prevention of gram-negative and gram-positive infections with 3 intravenous immunoglobulin preparations and therapy of experimental polymicrobial burn infection with intravenous Pseudomonas immunoglobulin G and ciprofloxacin in an animal model]. 311 21

EDTA and EGTA when used in conjunction with AgNO3 enhanced the antibacterial action of the latter significantly, so that strains of Klebsiella pneumoniae and Staphylococcus aureus resistant to 70 micrograms/ml of AgNO3 were observed to became sensitive to 10 micrograms/ml of this compound. The synergistic effect of EDTA appears to be due to a mechanism other than the removal of lipopolysaccharide from outer membrane, as its effect could be observed in even non-LPS containing gram positive S. aureus cells. Penicillamine, another potent chelator had an opposite effect so that it decreased the toxicity of silver ions.
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PMID:Effect of certain chelating agents on the antibacterial action of silver nitrate. 314 59

Monoclonal antibodies were raised against Barber antigen (Ba) of Salmonella typhi 0901. Antibodies produced to antigen 9 of group D salmonellae were used in double- and triple-sandwich antibody enzyme-linked immunosorbent assays (ELISAs) for detecting antigen 9 in urine and plasma specimens from three groups of patients and 49 controls. The triple-antibody ELISA detected the antigen in urine samples from 11 of 18 (65%) patients with hemoculture-proven typhoid (group 1) and 12 of 39 (31%) patients with clinical features compatible with typhoid but whose hemocultures were negative (group 2). This ELISA was negative in three patients from whom Salmonella paratyphi A, Escherichia coli, and Klebsiella pneumoniae (group 3) were isolated by hemoculture and in all healthy controls. The double-antibody sandwich ELISA was positive in 41 and 15% of urine samples from patients in groups 1 and 2, respectively, and was negative with samples from two patients from group 3 and all controls. The sensitivity and specificity compared with those for healthy controls were 65 and 100%, respectively, for the triple-antibody ELISA. Although as little as 7.8 ng of homologous lipopolysaccharide could be detected, background in clinical specimens prevented accurate interpretation of the detection of this antigen in serum. Results were best with urine specimens.
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PMID:Detection with monoclonal antibody of Salmonella typhi antigen 9 in specimens from patients. 318 27

Ribosomal preparations from Klebsiella pneumoniae, Haemophilus influenzae, Streptococcus pyogenes, and Streptococcus pneumoniae were investigated with respect to their activating capacity towards murine lymphoid cells. The proliferation of BALB/c spleen cells was induced in a dose-dependent fashion (from 1 to 100 micrograms/ml) by ribosomes of K. pneumoniae, H. influenzae, and S. pyogenes with a peak activity at 48 or 72 hr of culture. The majority of the blast cells induced by these ribosomal preparations were positive for surface-immunoglobulin (S-Ig) and negative for Thy 1.2. Furthermore, K. pneumoniae, H. influenzae, and S. pyogenes ribosomes induced the synthesis of IgM and some IgA. Cell proliferation and induction of IgM production were also demonstrated with the 3 ribosomal preparations using spleen cells from athymic nude (nu+/nu+) mice, Lyb-5-defective CBA/N spleen cells, B cell-enriched and T cell-depleted BALB/c spleen cell suspensions, as well as spleen cells from the Ips gene-deficient C3H/HeJ strain. Cell culture supernatants contained specific anti-ribosome IgM antibodies. Antibodies of other specificities (anti-sheep erythrocytes) were also demonstrated in supernatants from K. pneumoniae-stimulated cultures. Evidence against a possible role of contamination of K. pneumoniae and H. influenzae ribosomes by lipopolysaccharide- or lipid A-associated proteins in this effect is discussed. Ribosomes from S. pneumoniae did not induce 3H-thymidine incorporation nor Ig production. None of the 4 ribosomal preparations was found to stimulate T cell blastogenesis or to induce interleukin-2 production by naive BALB/c spleen cells. Finally, ribosomes from H. influenzae, S. pyogenes, S. pneumoniae but not those of K. pneumoniae stimulated interleukin-1 production by adherent spleen cells, from BALB/c mice.
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PMID:Induction of murine B cell proliferation and immunoglobulin synthesis by some bacterial ribosomes. 326 81

The R-form lipopolysaccharide (LPS) from Escherichia coli K-12, from which cationic material had been removed by electrodialysis and the pH of which had fallen to 3.6, formed a rough hexagonal lattice structure with the lattice constant of about 19 nm. The rough hexagonal structure was maintained in buffers at pH 5 or lower but disintegrated into the ribbon-like structures in buffers at pH 6 or higher. However, in the presence of 10 mM Mg2+, the hexagonal lattice structure was not disintegrated even at alkaline pH levels but conversely it became more dense. At pH 8.3 to 8.9, the hexagonal lattice structure with the shortest lattice constant (15 nm) was formed. The same optimal pH levels were obtained for formation of the dense hexagonal lattice structure (lattice constant, 14 to 15 nm) by the electrodialyzed LPS from Klebsiella pneumoniae strain LEN-111 (O3-:K1-). The ability of Mg2+ to induce formation of the dense hexagonal lattice structure of the K-12 LPS depends upon the presence of buffers showing the optimal pH levels, since a very high concentration of Mg2+ such as 500 mM was required for the lattice formation in distilled water. The amount of the magnesium bound to the K-12 LPS did not significantly differ throughout the pH range of 3 to 9. Therefore, the optimal pH range is another essential factor for formation of the dense hexagonal lattice structure of the LPS in addition to binding of the magnesium to the LPS.
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PMID:In vitro hexagonal assembly of R-form lipopolysaccharides: effect of pH on the Mg+2-mediated hexagonal assembly. 328 6


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