Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a previous study we demonstrated that lipopolysaccharide failed to elicit nonspecific resistance in C3H/He lipopolysaccharide low-responder mice against Klebsiella infection in contrast to its activity in a closely related histocompatible high-responder subline, C3HeB/Fe. Complete restoration of lipopolysaccharide-induced protection against 10(5) Klebsiella was obtained in the present study by transferring bone marrow from high-responder mice to the highly deficient C3H/He mice. The ability of C3H/He mice to clear and destroy bacteria in 5 h was also transferred by C3HeB/Fe marrow cells. In contrast, when high-responder C3HeB/Fe mice were reconstituted with low-responder bone marrow, the clearance and destruction of K. pneumoniae were similar to what is observed in the high-responder strain, but survival was only temporary. Collectively, our data show that the failure of C3H/He mice to respond to lipopolysaccharide with nonspecific immunity is due to a defect in two types of bone-marrow-derived cells--radioresistant and radiosensitive.
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PMID:Transfer by bone marrow cells of increased natural resistance to Klebsiella pneumoniae induced by lipopolysaccharide in genetically deficient C3H/He mice. 37 12

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

To provide a database for the development of an O-antigen-polysaccharide-containing vaccine against Klebsiella spp., we examined the O-antigen seroepidemiology of 378 Klebsiella clinical isolates collected prospectively in two university centers. Strains were typed by competitive enzyme-linked immunosorbent assay with rabbit antisera specific for serogroups O1 to O12 and monoclonal antibodies (MAbs) specific for serogroups O1, O2ab, O2ac, and the genus-specific core antigen. The numbers of isolates (percentages) of individual O serogroups were as follows: 148 (39.2) for serogroup O1, 40 (10.6) for serogroup O2ab, 4 (1.1) for serogroup O2ac, 89 (23.6) for serogroup O3, 2 (0.5) for serogroup O4, 32 (8.5) for serogroup O5, none for serogroups O7, O9, and O12, and 21 (5.6) for serogroup O11. Forty-two (11.1) of the strains were non-O-typeable. O-serogroup distributions were virtually identical between isolates from invasive infections and those from noninvasive infections or colonizations. A vaccine containing the O-specific polysaccharides of serogroups O1, O2ab, O3, and O5 would cover 82% of clinically occurring O-antigen specificities. Three hundred thirty-eight of 378 isolates (89.4%) reacted with the genus-specific MAb V/9-5, which recognizes an epitope of the outer core region of Klebsiella lipopolysaccharide. Antibodies directed against this epitope may represent a further alternative for O-antigen-targeted immunoprophylaxis of Klebsiella infections. These data support further experimental investigations on the protective potential of O-antigen-based vaccines and/or hyperimmune globulins in Klebsiella infection.
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PMID:O-antigen seroepidemiology of Klebsiella clinical isolates and implications for immunoprophylaxis of Klebsiella infections. 930 4

Klebsiella pneumoniae has been isolated from liver abscesses in patients with leukaemia or diabetes. The resistance of Klebsiella infection in lipopolysaccharide (LPS)-hyporesponsive mice is unclear. Female C3H/HeJ and C3H/HeN mice, 6-8 weeks old, were intraperitoneally (i.p.) injected with K. pneumoniae. The results showed that C3H/HeJ mice were 24 times more susceptible [lethal dose 50% (LD50) 250 colony-forming units] than C3H/HeN mice to K. pneumoniae infection. C3H/HeJ mice, uninfected or infected with K. pneumoniae, had higher liver interleukin (IL)-10 levels and IL-10 mRNA levels than C3H/HeN mice. Previously, pretreatment with IL-1beta and tumour necrosis factor-alpha (TNF-alpha) protected C3H/HeJ mice from lethal bacterial infection. Therefore the effects of pretreatment with IL-1beta and TNF-alpha or antimurine IL-10 antibody i.p. 1 hr before this infection in both strains of C3H mice were examined. Pretreatment with TNF-alpha or anti-IL-10 antibody enhanced the survival of both strains of mice. TNF-alpha, in combination with IL-1beta, enhanced the survival and bacterial clearance better than single pretreatment in C3H/HeJ mice. Anti-IL-10 antibody increased bacterial clearance and significantly reduced liver cytokine mRNA levels in C3H/HeJ mice more than it did in the controls during infection. These results indicate that exogenous cytokine modulation or neutralization of IL-10 enhance the resistance of LD50 infection in C3H/HeJ mice.
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PMID:Exogenous cytokine modulation or neutralization of interleukin-10 enhance survival in lipopolysaccharide-hyporesponsive C3H/HeJ mice with Klebsiella infection. 1046 38

This study was undertaken in order to determine whether proinflammatory cytokines are involved in a previously described protection against Klebsiella infection mediated by antilipopolysaccharide antibodies. BALB/c mice were infected intraperitoneally with a lethal challenge of Klebsiella pneumoniae Caroli. One group of mice was protected with monoclonal antibodies against lipopolysaccharide prior to infection and the second was not. We determined the number of colony-forming units at different time points in the blood of infected animals and paralleled them with plasma levels of five proinflammatory cytokines measured by enzyme immunoassays. Our results show that the two groups of animals tested expressed different plasma concentrations for all cytokines. The greatest difference was detected 24 hours after infection, with a higher production in the unprotected group. We concluded that a reduced cytokine production is partially responsible for the survival of protected animals.
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PMID:Proinflammatory cytokines in antilipopolysaccharide immunity against Klebsiella infections. 1603 Mar 91

The outcome of an infection depends on host recognition of the pathogen, hence leading to the activation of signaling pathways controlling defense responses. A long-held belief is that the modification of the lipid A moiety of the lipopolysaccharide could help Gram-negative pathogens to evade innate immunity. However, direct evidence that this happens in vivo is lacking. Here we report the lipid A expressed in the tissues of infected mice by the human pathogen Klebsiella pneumoniae. Our findings demonstrate that Klebsiella remodels its lipid A in a tissue-dependent manner. Lipid A species found in the lungs are consistent with a 2-hydroxyacyl-modified lipid A dependent on the PhoPQ-regulated oxygenase LpxO. The in vivo lipid A pattern is lost in minimally passaged bacteria isolated from the tissues. LpxO-dependent modification reduces the activation of inflammatory responses and mediates resistance to antimicrobial peptides. An lpxO mutant is attenuated in vivo thereby highlighting the importance of this lipid A modification in Klebsiella infection biology. Colistin, one of the last options to treat multidrug-resistant Klebsiella infections, triggers the in vivo lipid A pattern. Moreover, colistin-resistant isolates already express the in vivo lipid A pattern. In these isolates, LpxO-dependent lipid A modification mediates resistance to colistin. Deciphering the lipid A expressed in vivo opens the possibility of designing novel therapeutics targeting the enzymes responsible for the in vivo lipid A pattern.
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PMID:Deciphering tissue-induced Klebsiella pneumoniae lipid A structure. 2657 97

Strains of Klebsiella pneumoniae are frequently opportunistic pathogens implicated in urinary tract and catheter-associated urinary-tract infections of hospitalized patients and compromised individuals. Infections are particularly difficult to treat since most clinical isolates exhibit resistance to several antibiotics leading to treatment failure and the possibility of systemic dissemination. Infections of medical devices such as urinary catheters is a major site of K. pneumoniae infections and has been suggested to involve the formation of biofilms on these surfaces. Over the last decade there has been an increase in research activity designed to investigate the pathogenesis of K. pneumoniae in the urinary tract. These investigations have begun to define the bacterial factors that contribute to growth and biofilm formation. Several virulence factors have been demonstrated to mediate K. pneumoniae infectivity and include, but are most likely not limited to, adherence factors, capsule production, lipopolysaccharide presence, and siderophore activity. The development of both in vitro and in vivo models of infection will lead to further elucidation of the molecular pathogenesis of K. pneumoniae. As for most opportunistic infections, the role of host factors as well as bacterial traits are crucial in determining the outcome of infections. In addition, multidrug-resistant strains of these bacteria have become a serious problem in the treatment of Klebsiella infections and novel strategies to prevent and inhibit bacterial growth need to be developed. Overall, the frequency, significance, and morbidity associated with K. pneumoniae urinary tract infections have increased over many years. The emergence of these bacteria as sources of antibiotic resistance and pathogens of the urinary tract present a challenging problem for the clinician in terms of management and treatment of individuals.
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PMID:Epidemiology and Virulence of Klebsiella pneumoniae. 2699 97