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

Strains of Haemophilus influenzae isolated in The Netherlands between 1975 and 1984 from patients with meningitis were analysed in order to determine whether older patients are infected with particular types or subtypes of the organism. Of 1154 patients with H. influenzae meningitis 73 (6.3%) were more than 6 years of age. Thirty-one strains (42%) were of serotype b, one strain was of serotyped, one strain was of serotype f and 40 strains (55%) were non-typable. Twenty-eight type b strains were available for subtyping by analysis of the major outer-membrane proteins by sodium dodecylsulphate (SDS)-polyacrylamide gel electrophoresis (PAGE), by serotyping of their lipopolysaccharides and by biotyping. Twenty-one strains were outer-membrane protein subtype 1,24-lipopolysaccharide serotype 1 and 24 biotype I. Seventeen strains (61%) combined these characteristics. This percentage did not differ significantly from the percentage found for strains isolated from patients of all age groups (80%). The 32 non-typable H. influenzae strains analysed had different outer-membrane protein patterns as seen by SDS-PAGE. Five biotypes were found, among which biotype II was predominant (21/32). The results indicated that (i) patients more than 6 years of age were infected by subtypes of H. influenzae b strains which were not significantly different from the strains isolated from younger patients, (ii) non-typable strains of H. influenzae were much more common (55%) in the older age group than in the younger (1.2%) and (iii) that these non-typable strains were not of a particular subtype.
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PMID:Types and subtypes of 73 strains of Haemophilus influenzae isolated from patients more than 6 years of age with meningitis in The Netherlands. 349 69

The elaboration of type b capsule plays an important role in determining virulence of Haemophilus influenzae but the contribution of lipopolysaccharide to pathogenicity of this organism remains undefined. Using DNA from a virulent type b H. influenzae donor strain and a capsule-deficient recipient (Rd:01), we constructed capsular transformants having lipopolysaccharide characteristics either similar to (strain Rd/b+:01), or different from (strain Rd/b+:02), the recipient strain. These two type b transformants had similar type b capsule and outer membrane proteins. Comparative virulence studies in rats showed that strain Rd/b+:02 was more virulent than Rd/b+01 as assessed by magnitude of bacteraemia, incidence of meningitis and mortality. Similarly, strain Rd/b-:02 exhibited greater pathogenicity in C3-depleted rats than its genetically-related strain Rd:01. We conclude that lipopolysaccharide composition plays a significant role in mediating the potential of H. influenzae to cause invasive infections. In addition, the findings suggest that there is linkage of virulence genes involved in lipopolysaccharide and capsule expression.
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PMID:Contribution of lipopolysaccharide to pathogenicity of Haemophilus influenzae: comparative virulence of genetically-related strains in rats. 350 84

Epidemiological data show that O18:K1 Escherichia coli is a common cause of neonatal bacteremia and meningitis. These bacteria were capable of multiplying in the bloodstream of newborn rats and were resistant to the bactericidal effects of complement in the absence of specific antibodies. The roles played by the O antigen and the K antigen in complement resistance were analyzed by comparing the bactericidal effects of normal sera and of sera deficient in various complement components or in immunoglobulins. These sera were tested on O18:K1 bacteria and on mutants lacking either the lipopolysaccharide O antigen or the K1 capsular polysaccharide. In addition, O1:K1 cells, which can cause pyelonephritis but which are rare in newborn meningitis and which do not multiply in the bloodstream of newborn rats, were also examined. Different mechanisms of protection against the alternative and classical pathways were recognized: K1-positive cells were resistant to the bactericidal activity of sera deficient in classical complement pathway components, whereas K1-negative cells were sensitive to these sera. Based on these results and on those from complement fixation assays, the K1 sialic acid polysaccharide impedes the activation of, and thus protects the bacteria against, the alternative complement pathway. Not only the K1-negative mutant cells but also O1:K1 bacteria and mutants lacking the O18 oligosaccharide repeating units of the lipopolysaccharide were sensitive to the classical complement pathway. These bactericidal effects were observed even in the absence of specific antibodies. It is proposed that both the K1 capsule and the O18 oligosaccharide restrict antibody-independent classical pathway activation by shielding deeper structures on the cell membrane that are capable of activating this pathway.
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PMID:Role of the capsule and the O antigen in resistance of O18:K1 Escherichia coli to complement-mediated killing. 619 96

Eighty strains of Haemophilus influenzae type b were randomly selected from 531 strains collected between 1975 and 1982 from patients with meningitis in The Netherlands. Subtyping by sodium dodecyl sulfate-polyacrylamide gel electrophoresis revealed that 67 of 80 isolates had identical major outer membrane protein patterns (subtype 1). Among the 13 other isolates four different polyacrylamide gel electrophoresis patterns were observed, two of which closely resembled subtype 1. Lipopolysaccharides were characterized immunologically by immunoprecipitation (Ouchterlony technique) and the gel-immuno-radio-assay. Four serotypes were found among the 80 selected strains, leaving one strain not typable. Seventy-four strains (93%) belonged to the same lipopolysaccharide serotype; 77 (97%) of 80 of the strains belonged to biotype I. Sixty strains (75%) had identical major outer membrane protein patterns (subtype 1), lipopolysaccharide serotypes (serotype 1), and biotypes (I).
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PMID:Homogeneity of cell envelope protein subtypes, lipopolysaccharide serotypes, and biotypes among Haemophilus influenzae type b from patients with meningitis in The Netherlands. 641 28

Levels of serum antibodies to lipopolysaccharide (LPS) were measured in acute- and convalescent-phase sera from 27 patients with meningitis due to Haemophilus influenzae type b using an enzyme-linked immunosorbent assay. The geometric mean titers of antibodies to LPS in acute-phase sera were similar to those of 24 control children and 22 healthy adults. In convalescent-phase sera there was a fourfold increase in the geometric mean titers of IgG and IgM antibodies to LPS. The antibody responses wee independent of age and of antibody response to the type b capsule. However, the responses were bimodal: children with high levels of IgG and IgM antibodies to LPS in acute-phase sera did not respond with further increases in serum antibodies to LPS after infection, whereas children with lower initial levels showed high responses. The presence of high levels of antibodies to LPS in the sera of half of the acutely ill children suggests that antibodies to some LPS determinants are not protective.
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PMID:Human antibody responses to lipopolysaccharide after meningitis due to Haemophilus influenzae type b. 697 94

A polysaccharide-protein complex prepared from Haemophilus influenzae type b strain Eagan was used as test antigen in an enzyme-linked immunosorbent assay for human serum antibodies. With washing buffer that did not contain detergent, the assay detected antibody to lipopolysaccharide (LPS) and to non-LPS somatic antigens as well as to polyribosylribitolphosphate (PRP. With buffer that did contain detergent, antibodies to LPS were not detected, whereas detection of antibodies to the non-LPS somatic components and to PRP wa unimpeded. Similarly, purified LPS could be used as test antigen with the former buffer only. IgG, IgA, and IgM antibodies to non-LPS somatic antigens were prevalent in healthy adults and children, and levels increased in 14 of 15 patients recovering from meningitis due to H. influenzae type b; IgG was the predominant class. Antibodies to LPS were prevalent but at lower concentrations, and IgM was the predominant class; levels increased in 12 of the 15 patients.
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PMID:A polysaccharide-protein complex from Haemophilus influenzae type b. II. Human antibodies to its somatic components. 697 2

Tumor necrosis factor-alpha (TNF-alpha) is a pathogenic factor in bacterial meningitis. The effect of thalidomide on TNF-alpha production by microglia, the resident macrophages of the brain, was evaluated. In primary human fetal microglial cell cultures stimulated with lipopolysaccharide or lipoarabinomannan, thalidomide inhibited TNF-alpha release in a dose-dependent manner. The inhibitory effect of thalidomide was similar to that of dexamethasone, although expression of TNF-alpha mRNA in microglial cells was reduced only by thalidomide. The results of this in vitro study suggest that thalidomide could have therapeutic potential in gram-negative bacterial and tuberculous meningitis.
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PMID:Thalidomide inhibits tumor necrosis factor-alpha production by lipopolysaccharide- and lipoarabinomannan-stimulated human microglial cells. 756 Nov 98

Alterations in the blood-brain and blood-cerebrospinal fluid barriers occur during bacterial meningitis. Preventing barrier alterations is important as the increases in barrier permeability are thought to contribute to adverse neurological outcomes. The objective of this study was to characterize pharmacokinetically cerebrovascular permeability alterations during meningeal inflammation. 14C-Sucrose was used as a quantitative marker of cerebrovascular integrity 8 hr after induction of experimental meningitis by intracisternal injection of 0, 25 or 200 micrograms lipopolysaccharides. Serum and brain tissues were obtained after tracer dosing. 14C-Sucrose influx transfer coefficients (Kin(app)) and cerebrovascular volumes (Vbr) were calculated for each brain region. Regional Vbr values were unaffected by lipopolysaccharide pretreatment. However, statistically significant increases in 14C-sucrose K(in)(app) values were observed in various brain regions (1.6- to 3.3-fold from control; P < .05). These permeability alterations cannot be attributed to changes in the systemic pharmacokinetics of 14C-sucrose as total clearance and the volume of distribution were unaffected by lipopolysaccharide treatment. This approach can be used in future studies to examine the contribution of various inflammatory mediators to altered cerebrovascular permeabilities during experimental meningitis.
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PMID:Cerebrovascular permeability changes during experimental meningitis in the rat. 756 88

The mechanism underlying meningitis-associated brain injury is unclear. This study investigated the hypothesis that lipopolysaccharide (LPS) alters astrocyte function and structure via the release of proinflammatory cytokines. In enriched murine astrocyte cultures, LPS inhibited (P < 0.05) glutamine synthetase activity, 3H-gamma aminobutyric acid uptake, and DNA synthesis; LPS also induced ultrastructural changes. Antibodies to tumor necrosis factor-alpha, interleukin-1, and interleukin-6 blocked (P < 0.05) in part the LPS-induced inhibition of astrocyte function. Also, treatment of astrocyte cultures with cytokines significantly altered these astrocyte functions and ultrastructure. Taken together, the present findings support the hypothesis that LPS affects astrocyte function and structure via the release of proinflammatory cytokines, especially tumor necrosis factor-alpha.
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PMID:Role of cytokines in lipopolysaccharide-induced functional and structural abnormalities of astrocytes. 791 Aug 8

Nitric oxide (NO) is produced by murine macrophages in response to cytokines and/or gram-negative bacterial lipopolysaccharide. NO induction by gram-positive bacteria such as group B streptococci (GBS), the major etiologic agents of neonatal pneumonia and meningitis, has received little study. GBS as well as two other gram-positive bacterial species, Staphylococcus aureus and Staphylococcus epidermidis, were found to stimulate NO production in thioglycolate-elicited murine macrophages and in the mouse macrophage cell line J774A.1 in the presence of gamma interferon. Serotype Ia and III GBS were both stimulatory, as were asialo- and type antigen-deficient mutant strains of type III GBS. NO production was dose dependent, inhibitable by L-arginine analogs, and unaffected by polymyxin B. Since phagocytosis by murine and human phagocytes of GBS is dependent on complement receptor type 3 (CR3), the role of CR3 in the NO response to GBS was tested in the CR3-deficient myelomonocytic cell line WEHI-3. GBS did not induce NO, whereas S. aureus or lipopolysaccharide did induce NO in WEHI-3 cells. S. epidermidis, whose nonopsonic phagocytosis is also CR3 dependent, failed to induce NO in WEHI-3 cells. Monoclonal anti-CR3 (anti-CD11b or anti-CD18) in the presence of interferon also induced NO production in thioglycolate-elicited macrophages and in J774A.1 cells but not in WEHI-3 cells. This evidence suggests that ligated CR3 and gamma interferon act synergistically to induce NO production and that CR3 mediates the GBS-induced signal for NO production in interferon-treated macrophages.
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PMID:Group B streptococcus-induced nitric oxide production in murine macrophages is CR3 (CD11b/CD18) dependent. 803 77


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