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

The high-molecular fraction of substances of the cell wall of meningococci, groups A and B, isolated in free volume in gel filtration through sepharose 4B and containing both group and intergroup antigens proved to be consisting of 2 subfractions in gel-filtration through Bio-Gel A-150m. Molecular weight of the first was within the range of 100--150 million dalton, and of the second--of 3 to 100 million dalton. In dissociation in sodium deoxycholate the high molecular fraction complex compound of the cell wall of meningococcus strain, group A, isolated from the cerebrospinal fluid of a patient suffering from meningitis broke down into 5 fragments differing in chemical nature and mol wt. There were revealed protein and protein-lipopolysaccharide components with a relatively high mol wt. polypeptide components and low molecular residues of the initial lipopolysaccharide.
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PMID:[Study of molecular heterogeneity and chemical nature of polymeric components of the Meningococcus cell wall]. 9 83

Although Escherichia coli strains possessing the K1 capsule are predominant among isolates from neonatal E. coli meningitis and most of these K1 isolates are associated with a limited number of 0 lipopolysaccharide (LPS) types, the basis of this association of K1 and certain 0 antigens with neonatal E. coli meningitis is not clear. The present study examined in experimental E. coli bacteremia and meningitis in newborn and adult rats whether or not the K1 capsule and/or O-LPS antigen are critical determinants in the development of meningitis. Rats received subcutaneously at K1 E. coli strain (018+K1+) or mutants lacking either the K1 capsule (018+K1-) or 0 side-chain (018-K1+). 12-24 h later, blood and cerebrospinal fluid (CSF) specimens were obtained for quantitative cultures. The isolation of E. coli from CSF was observed in both newborn and adult rats infected with K1+ strains regardless of LPS phenotype (018+ or 18-) who also developed a high degree of bacteremia (e.g., greater than 10(4) CFU/ml of blood). In contrast, none of the newborn and adult rats infected with 018+K1- and developing bacteremia of greater than 10(4) were found to have positive CSF cultures. These findings indicate that the presence of the K1 capsule and a high degree of bacteremia are key determinants in the development of E. coli meningitis, suggesting that there may be specific binding sites present in the brain which have an affinity for the K1 capsule and thus may be responsible for the entry of K1-encapsulated E. coli into the meninges.
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PMID:The K1 capsule is the critical determinant in the development of Escherichia coli meningitis in the rat. 132

An in vitro blood-brain barrier (BBB) model consisting of primary cultures of bovine brain microvascular endothelial cells was used to examine the effect of Haemophilus influenzae type b (Hib) on the BBB. Whole bacteria and purified lipopolysaccharide (LPS; greater than 10 ng/ml) caused marked cytotoxicity on the bovine brain endothelial cells. This effect could be completely blocked by polymyxin B. Similar cytotoxic effects were observed with a cultured bovine pulmonary endothelial cell line. Serum was essential for the LPS-mediated cytotoxic effect, and human, horse, bovine, or fetal calf serum all had similar effects. The serum factor was not a complement component. A monoclonal antibody against CD14, a receptor involved in mediating the effect of LPS in monocytes, completely blocked the cytotoxic effect in both brain and pulmonary endothelial cells. These results suggest that Hib LPS disrupts an in vitro BBB model via a serum- and CD14-dependent pathway and that LPS has cytotoxic effects on bovine endothelial cells without the involvement of monocytic cells, an effect that may be important in gram-negative meningitis and in endotoxic shock.
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PMID:Haemophilus influenzae lipopolysaccharide disrupts confluent monolayers of bovine brain endothelial cells via a serum-dependent cytotoxic pathway. 137 54

The class 1 outer membrane protein of Neisseria meningitidis B:15:P1.7,16 was expressed in Bacillus subtilis in high yield as intracellular aggregates. These were easy to isolate and the protein (called BacP1) could be solubilized under denaturing conditions. Sera of mice immunized with thus-solubilized BacP1 contained high titres of antibodies that reacted with the class 1 protein of the meningococcal envelope in immunoblots but did not react with native meningococcal envelope in enzyme immunoassays (EIA) or with intact meningococci in bactericidal assays. However, when the BacP1 protein was complexed with heterologous (Salmonella) lipopolysaccharide, the ensuing sera reacted with meningococcal envelope preparations in both EIA and immunoblots, showed subtype-specific bactericidal activity, and were protective in an infant rat meningitis model.
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PMID:The class 1 outer membrane protein of Neisseria meningitidis produced in Bacillus subtilis can give rise to protective immunity. 140 85

In animal models, the lipopolysaccharide (LPS) from Haemophilus influenzae contributes to all the signs of meningitis associated with living bacteria. However, when tested in vitro, the amount of LPS in cerebrospinal fluid (CSF) in natural disease shows much greater effects on leukocytes than on endothelial permeability. To investigate whether other bacterial components act with LPS to incite meningeal inflammation, animals were challenged intracisternally with H. influenzae lysates. Upon neutralization of endotoxin, leukocytosis was greatly attenuated, but protein accumulation in CSF persisted. Cell wall from H. influenzae induced meningeal inflammation in a pattern opposite to that of LPS. Its ability to induce blood-brain barrier permeability greatly exceeded its ability to induce leukocytosis in vivo. Thus, cell wall, by acting on endothelia, and LPS, by inducing leukocytosis, may cooperate to induce inflammation in H. influenzae meningitis. Optimal reduction of inflammation and tissue damage in meningitis may require agents directed against cell wall as well as LPS.
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PMID:Bacterial components and the pathophysiology of injury to the blood-brain barrier: does cell wall add to the effects of endotoxin in gram-negative meningitis? 158 87

Injury to the blood brain barrier (BBB) is a fundamental sequela of bacterial meningitis, yet the precise mechanism facilitating exudation of albumin across the endothelium of the cerebral microvasculature remains conjectural. After intracisternal inoculation of Escherichia coli (0111:B4) lipopolysaccharide in rats to elicit a reversible meningitis and BBB injury, we utilized in situ tracer perfusion and immunolabeling procedures to identify by transmission electron microscopy the precise topography and microvascular exit pathway(s) of bovine serum albumin (BSA). Results revealed that during meningitis there was: (a) an inducible increase in immunodetectable monomeric BSA binding to the luminal membrane of all microvascular segments in the pia-arachnoid and superficial brain cortex; (b) similar uptake of both colloidal Au-BSA (as well as monomeric BSA) by plasmalemmal vesicles but no detectable transcytosis to the abluminal side; and (c) predominant exit of both perfused Au-BSA and immunodetectable monomeric BSA through open intercellular junctions of venules in the pia-arachnoid. This was corroborated in separate experiments documenting focal pial venular leaks of in situ perfused 0.01% colloidal carbon black during experimental meningitis. These results provide precise localization of BBB injury in meningitis to meningeal venules, confirm a paracellular exit pathway of albumin via open intercellular junctions, and suggest an injury mechanism amenable to specific therapeutic intervention.
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PMID:Ultrastructural localization of albumin transport across the cerebral microvasculature during experimental meningitis in the rat. 187 66

The incidence, case fatality rate (CFR), age distribution, serotype distribution and transmission of Haemophilus influenzae meningitis worldwide are reviewed. This organism is a commensal in the throat, but serotype b can become invasive and causes the majority of meningitis disease in infants in most countries. The incidence is estimated at 47/100,000 in the US, and 20-30/100,000 in Europe for children 5 years. In non-industrialized settings, data are available for Alaska and The Gambia, where incidence is 60/100,000 children 5. In Africa the peak age is 6 months of age, compared to 8-9 months is the West, where 60% of cases occur in adults as well. The CFR ranges from 1.95-5% in the West, a function of hospital facilities, but is reported to be 26% in Nigeria and 57% in Egypt. H. influenzae serotype b predominates in most countries. Only 3 common outer membrane protein antigens are common, but the lipopolysaccharide types vary widely. In West Africa serotype a is more prevalent, and in The Gambia an entirely different clone was isolated. The carriage rate appears to be low, around 2-4% in most communities, but in some closed communities, such as day care centers, up to 56% carriage has been found. It is theorized that introduction of new strains is the reason for infection of very young children in developing areas.
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PMID:World-wide epidemiology of Haemophilus influenzae meningitis; industrialized versus non-industrialized countries. 189 57

Twenty-four Haemophilus influenzae type b strains from 836 children and young adults in an open population were subtyped by outer-membrane-protein (OMP) analysis on sodium dodecyl sulphate-polyacrylamide gels, lipopolysaccharide serotyping and biotyping. The results were compared with those obtained with H. influenzae type b strains from 97 patients with meningitis in the same city (Amsterdam). OMP subtype 1 was significantly more common among the CSF isolates than in carrier strains (82% vs 50%; p less than 0.002). The other OMP subtypes found among carriers were rarely isolated from patients. The lipopolysaccharide serotype and biotype distribution did not differ between the two groups. The combination of OMP subtype 1, lipopolysaccharide 1, biotype I was much more common in isolates from patients than in those from carriers (71% vs 42%; p less than 0.01). The data suggest that various H. influenzae type b subtypes are less virulent than those commonly isolated from invasive infections.
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PMID:Differences in subtype distribution of Haemophilus influenzae type b from carriers in the general population and patients with meningitis. 205 15

A prospective nationwide surveillance of invasive Haemophilus influenzae type b disease among adults (greater than or equal to 16 years old) was conducted in Finland during 1985 through 1988. Thirty-one cases were identified (annual incidence, 0.22/100,000). Of these infections, 71% occurred in patients with severe underlying conditions. The overall case fatality rate was 26%. Septicemia (13 patients) and pneumonia (seven patients) were the most common clinical manifestations of H influenzae type b infection; the others were epiglottitis (six patients), meningitis (three patients), and arthritis (two patients). Epiglottitis occurred in significantly younger patients, all of whom were women and four of whom were previously healthy. Subtyping of the H influenzae type b isolates according to the major outer membrane protein subtype, biotype, and lipopolysaccharide serotype showed that patterns that were uncommon (14%) among children were more common (27%) in the adults.
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PMID:Spectrum of invasive Haemophilus influenzae type b disease in adults. 224 74

Interleukin-1 (IL-1) is the key initiator of host responses to infection. We describe here the lipopolysaccharide-(LPS) (20 micrograms/ml) stimulated IL-1 production of peripheral blood monocytes in 2 children with Haemophilus influenzae meningitis. We found a depressed IL-1 production at the acute stage of the infection when the meningitis was most active with return to normal coinciding with clinical recovery. These results show an inverse correlation with acute phase reactants and IL-1 production. Normalization of IL-1 production seems to be a good prognostic sign in bacterial meningitis.
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PMID:Interleukin-1 production in bacterial meningitis. 232 Sep 58


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