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

Strains of Pseudomonas aeruginosa initially isolated from patients with cystic fibrosis (CF) often express a smooth lipopolysaccharide (LPS) containing many long O side-chain antigens, but once a chronic infection is established, strains recovered from these patients express little or no LPS O antigen. The genetic basis for this loss of O antigen expression by P. aeruginosa CF isolates is unknown. We report here that 20 CF isolates of P. aeruginosa, 13 of which are LPS-rough, were each capable of expressing serogroup O11 antigen when provided with the rfb locus from P. aeruginosa serogroup O11 strain PA103 on the recombinant plasmid pLPS2. Eight of the thirteen LPS-rough isolates co-expressed another, presumably endogenous, O antigen when they contained pLPS2. Different subcloned regions of pLPS2 complemented distinct strains to restore endogenous O antigen expression. These data suggest that the loss of O antigen expression by P. aeruginosa CF isolates results from alterations specific to the rfb region, and is not due to mutations involving other loci or ancillary LPS genes.
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PMID:The rfb locus from Pseudomonas aeruginosa strain PA103 promotes the expression of O antigen by both LPS-rough and LPS-smooth isolates from cystic fibrosis patients. 752 92

Multi-resistant strains from three UK centres, previously identified as Burkholderia (formerly Pseudomonas) cepacia, and associated with morbidity, mortality and transmission among patients with cystic fibrosis have been further characterised. Biochemical tests and fatty acid analyses indicate these strains to possess some characteristics atypical of B. cepacia but bearing close resemblance to Burkholderia gladioli, an organism previously regarded solely as a plant pathogen and a hindrance to the identification of B. cepacia. In contrast to the majority of reference strains, all multi-resistant clinical isolates possessed rough lipopolysaccharide which may be a major factor responsible for their increased antibiotic resistance and virulence. In view of the potential clinical and social problems in CF patients posed by these multi-resistant strains, it would seem prudent to consider the isolation of either B. cepacia or B. gladioli as of equal significance.
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PMID:Multi-resistance isolates possessing characteristics of both Burkholderia (Pseudomonas) cepacia and Burkholderia gladioli from patients with cystic fibrosis. 753 Feb 42

Burkholderia cepacia (Pseudomonas cepacia) is now recognised as an important pathogen in cystic fibrosis patients, and several reports have suggested that sputum-culture-proven colonisation occurs despite the presence of specific antibody. In an attempt to establish the use of antibody studies as diagnostic and prognostic indicators of B. cepacia infection, we have examined the IgG response to B. cepacia outer membrane proteins and lipopolysaccharide in patients also colonised with P. aeruginosa. The B. cepacia strains were grown in a modified iron-depleted chemically defined medium and outer membrane components examined by SDS-PAGE and immunoblotting. IgG antibodies were detected against B. cepacia outer membrane antigens, which were not diminished by extensive preadsorption with P. aeruginosa. The response to B. cepacia O-antigen could be readily removed by adsorption of serum either with B. cepacia whole cells or purified LPS, whereas we were unable to adsorb anti-outer membrane protein antibodies using B. cepacia whole cells. The inability to adsorb anti-outer membrane protein antibodies using B. cepacia whole cells maybe due to non-exposed surface epitopes. Several B. cepacia sputum-culture negative patients colonised with P. aeruginosa had antibodies directed against B. cepacia outer membrane protein. this study suggests that there is a specific anti-B. cepacia LPS IgG response, which is not due to antibodies cross-reactive with P. aeruginosa. Our studies indicate that much of the B. cepacia anti-outer membrane protein response is specific and not attributable to reactivity against co-migrating LPS.
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PMID:Serum IgG response to Burkholderia cepacia outer membrane antigens in cystic fibrosis: assessment of cross-reactivity with Pseudomonas aeruginosa. 753 70

Burkholderia cepacia has emerged as an important multiresistant pathogen in cystic fibrosis (CF), associated in 20% of colonised patients with a rapid and fatal decline in lung function. Although knowledge of B. cepacia epidemiology has improved, the mechanisms involved in pathogenesis remain obscure. In this study, B. cepacia lipopolysaccharide (LPS) was assessed for endotoxic potential and the capacity to induce tumour necrosis factor (TNF). LPS preparations from clinical and environmental isolates of B. cepacia and from the closely related species Burkholderia gladioli exhibited a higher endotoxic activity and more pronounced cytokine response in vitro compared to preparations from the major CF pathogen Pseudomonas aeruginosa. This study help to explain the vicious host immune response observed during pulmonary exacerbations in CF patients colonised by B. cepacia and lead to therapeutic advances in clinical management.
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PMID:Biological activity of Burkholderia (Pseudomonas) cepacia lipopolysaccharide. 764 Jun 78

In a rat model of chronic Pseudomonas aeruginosa lung infection mimicking cystic fibrosis, we investigated the possibility of preventing chronic lung inflammation or decreasing the progression of the infection. We compared the lethality, pathology, bacterial clearance, and immunogenicity after stimulation of the non-specific defence mechanisms by Escherichia coli lipopolysaccharide (LPS) or P. aeruginosa sonicate, or the acquired specific immune response by vaccination with the same bacterial antigens. One day prior to challenge with P. aeruginosa embedded in alginate beads, rats were stimulated with either E. coli LPS or P. aeruginosa sonicate. Four and two weeks prior to challenge other rats were vaccinated with either E. coli LPS or P. aeruginosa sonicate. Controls did not receive any stimulation or vaccination. The lethality after challenge was lower in rats stimulated with E. coli LPS (p = 0.02) or vaccinated with P. aeruginosa sonicate (p = 0.03) as compared to controls. The histopathology of the surviving rats showed an acute inflammation dominated by polymorphonuclear leukocytes (PMNs), but the offending bacteria were not completely eliminated in any group. The increased survival was probably due to earlier recruitment of PMNs most likely mediated by either cytokines and other chemotactic factors (stimulated group) or the immune response in concert with the complement cascade (vaccinated group). The results of the present and previous vaccination studies show that it is possible to improve survival but not to prevent the chronic P. aeruginosa lung infection and inflammation caused by alginate-embedded bacteria.
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PMID:Experimental chronic Pseudomonas aeruginosa lung infection in rats. Non-specific stimulation with LPS reduces lethality as efficiently as specific immunization. 765 61

Micromethods were developed to extract lipopolysaccharide (LPS, endotoxin) from single bacterial colonies of the 20 recognized Pseudomonas aeruginosa type strains. The appearance of these LPSs in polyacrylamide gel electrophoresis (PAGE) and their reactivity with serum of cystic fibrosis (CF) patients chronically infected with P. aeruginosa was studied. Silver staining of LPS after PAGE showed that 13 of the P. aeruginosa LPSs had high numbers of O-repeating units arranged in 1-4 clusters of banding. Low-molecular-weight LPS fractions were more prominent in six of the serotype strains, of which O:7 and O:14 appeared semi-rough. Corresponding immunoblots using the CF sera showed LPS patterns very similar to the silver-stained appearance, indicating an immune reaction to all P. aeruginosa LPS including that from the newly discovered O:18, O:19 and O:20. This was unexpected since only a few serotype strains (mostly O:3, O:6 and O:9) had been isolated from the patients. Absorption experiments using purified and chemically defined P. aeruginosa rough LPS and smooth LPS suggested these immune reactions were due to antibodies cross-reactive to core/lipid A as well as to lower molecular weight O-polysaccharides or "A-bands". However, in some cases O:3, O:6, and O:9 LPSs were also found to contain additional distinct O-epitopes. Immune recognition of various polyagglutinable P. aeruginosa LPSs seemed also to be caused by cross-reactive antibodies. The described microextraction methods, followed by PAGE and silver staining or immunoblotting, are easy and convenient techniques with which to study antibodies against LPS epitopes and to screen for LPS phenotypic appearance using only a few bacterial colonies from larger numbers of Gram-negative bacterial strains.
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PMID:Antibodies from chronically infected cystic fibrosis patients react with lipopolysaccharides extracted by new micromethods from all serotypes of Pseudomonas aeruginosa. 768 90

The immunological response of cystic fibrosis (CF) patients to lipopolysaccharide (LPS) antigens of Pseudomonas cepacia was investigated. Enzyme-linked immunosorbent assays (ELISA) with either P. cepacia whole cells or extracted core LPS from a clinical isolate of P. cepacia as antigen were used to measure serum IgG and sputum IgA anti-P. cepacia antibodies. The ELISA with core LPS distinguished nine CF patients colonised by P. cepacia from nine age- and sex-matched non-colonised CF patients. The rate of increase of anti-P. cepacia IgG antibodies after bacteriologically proven P. cepacia colonisation varied in individual patients: in some patients the first isolation of P. cepacia was preceded or accompanied by a two-to-four-fold rise in anti-P. cepacia LPS IgG titres. Absorption studies and immunoblot analysis of serum from patients colonised with P. cepacia demonstrated that a significant component of the anti-P. cepacia core LPS antibodies was specific for P. cepacia and did not react with the core LPS of P. aeruginosa. Immunoblotting also illustrated that there may be a degree of core heterogeneity between different isolates of P. cepacia. Detection of P. cepacia LPS specific antibodies in serum (IgG) and sputum (IgA) from CF patients is recommended to assist the identification of P. cepacia colonisation in CF patients.
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PMID:Serum IgG and sputum IgA antibody to core lipopolysaccharide antigen from Pseudomonas cepacia in patients with cystic fibrosis. 768 77

Cystic fibrosis (CF) patients suffer from many of the gastrointestinal conditions which occur in non-CF individuals, e.g., dyspepsia and peptic ulceration. These symptoms may be caused by Helicobacter pylori but could also be due to either pancreatic insufficiency or the intensive antibiotic treatment used in CF patients. Since CF patients chronically infected with Pseudomonas aeruginosa produce antibodies against a wide range of antigens, including antigens common to many other bacteria, e.g., GroEL and lipopolysaccharide, we studied, by the Western blot (immunoblot) technique, the specificity of immunoglobulin G antibodies to H. pylori in Danish CF patients chronically infected with P. aeruginosa, CF patients without P. aeruginosa infection but with Haemophilus influenzae infection, patients with dyspeptic ulcers associated with H. pylori, and patients recovering from acute Campylobacter jejuni or Campylobacter coli infection. Sera from CF patients with chronic P. aeruginosa or H. influenzae infection and patients recovering from acute C. jejuni infection cross-reacted with H. pylori antigens. A strong cross-reacting protein antigen at approximately 14 kDa and minor cross-reactive antigens at approximately 27, 30, and 60 kDa (the heat shock protein GroEL is equivalent to the common antigen of P. aeruginosa) could be demonstrated. The results of this study show that high immunoglobulin G antibody titers against H. pylori in CF patients cannot be regarded as indicating present or past H. pylori infection unless their specificity is proven by absorption studies.
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PMID:Cross-reactive antigens shared by Pseudomonas aeruginosa, Helicobacter pylori, Campylobacter jejuni, and Haemophilus influenzae may cause false-positive titers of antibody to H. pylori. 769 22

The aim of the present thesis was to summarize some important immunological mechanisms in the pathogenesis of chronic Pseudomonas aeruginosa lung infection in patients with cystic fibrosis (CF). The continuous presence of bacteria in the lungs induce a strong immunological response in the patients both locally in the lungs and systemically with high amounts of circulating specific anti-P. aeruginosa antibodies. Our work has been concentrating on anti-lipopolysaccharide (LPS) antibodies. We have shown an increasing antibody response in CF patients, to all three parts of the LPS molecule; lipid A, core, and O-sugars, during the course of chronic P. aeruginosa infection. The antibodies belonged to both IgA, IgM, and all four subclasses of IgG, and were detected in serum and sputum. We detected immune complexes (IC)s in sputum from chronically infected CF patients. The ICs were composed of P. aeruginosa LPS and immunoglobulins of both IgG1-4, IgA and IgM. The concentration of circulating ICs were significantly higher in chronically infected patients compared to non-infected CF patients. The presence of ICs containing LPS in sputum were positively correlated to the amount of tumor necrosis factor alpha (TNF alpha) in the same sputum sample. TNF alpha is a very potent inflammatory mediator, stimulating cells for release of several cytokines attracting polymorphonuclear neutrophil granulocytes (PMNs), which release proteolytic enzymes and toxic oxygen radicals. We detected high concentrations of both TNF alpha, interleukin (IL)-1 alpha, IL-1 beta, IL-6, and the IL-1 receptor antagonist (IRAP) in sputum from chronically infected CF patients. The corresponding concentrations of the cytokines in serum were low or undetectable. Relatively high concentrations of serum-IRAP before the diagnosis of chronic P. aeruginosa infection were correlated to development of poor pulmonary function. We made ICs in vitro of purified P. aeruginosa LPS and hyperimmune serum from chronically infected CF patients. The biological activity of these ICs was investigated in two different assays. LPS by itself induced TNF alpha liberation in vitro, but the ICs made in vitro were also able to stimulate TNF alpha release from mononuclear cells, and they were a more potent stimuli compared to the corresponding amount of LPS alone. The IC preparation did also induce an oxidative burst response in PMNs. We conclude P. aeruginosa LPS is biological active and formation of ICs involving P. aeruginosa LPS and anti-LPS antibodies takes place in the lungs of chronically infected CF patients.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Lipopolysaccharide (LPS), LPS-immune complexes and cytokines as inducers of pulmonary inflammation in patients with cystic fibrosis and chronic Pseudomonas aeruginosa lung infection. 775 34

Typing methods in seven laboratories were compared for their ability to type reproducibly 200 strains of Pseudomonas aeruginosa, predominantly from patients with cystic fibrosis (CF). Methods included lipopolysaccharide (LPS) serotyping, phage susceptibility typing, bacteriocin production, pilin gene typing, and analysis by restriction fragment length polymorphism (RFLP) with a probe upstream from the exotoxin A gene. The methods differed substantially in their capacity to identify unique typing patterns and to type each strain reproducibly on three occasions. For strains from patients with CF, the RFLP typing method had the greatest discriminatory power (30 unique patterns, 105 [70%] of 150 typed reproducibly). LPS serotyping appeared to be equivalent to RFLP typing for discriminating among P. aeruginosa strains from the environment and from clinical sources other than CF patients. RFLP analysis appears to be the best method for typing P. aeruginosa strains with rough LPS (such as from patients with CF). LPS serotyping appears preferable for other indications as it is simpler to perform.
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PMID:A multicenter comparison of methods for typing strains of Pseudomonas aeruginosa predominantly from patients with cystic fibrosis. The International Pseudomonas aeruginosa Typing Study Group. 790 73


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