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)

We studied a previously healthy 20-year-old woman who presented with gonococcal meningitis. The gonococcal isolate, HT-1, was prototrophic by auxotyping, was protein I serovar IB-1, and agglutinated with wheat germ lectin. This isolate differed from the proline-requiring, serovar IA-1 and IB-4, wheat germ-agglutination-negative gonococcal isolates recovered from three patients during a recent outbreak of gonococcal meningitis in Philadelphia. HT-1 was killed by normal pooled human sera (greater than or equal to 98% at 30 min) but not effectively killed by the convalescent-phase sera of the patient (greater than 30% survival at 30 min). Similar results were obtained when mucosal and cerebrospinal fluid isolates from a Philadelphia patient were exposed to these sera, but mucosal and blood isolates from another Philadelphia case showed increased resistance to killing by normal pooled human sera. Further characterization revealed multiple differences in outer membrane and cellular proteins and lipopolysaccharide between case isolates. Absence of the L8 lipopolysaccharide epitope was noted for all isolates. Sera of our patient were found to have low total hemolytic complement (CH100 = 21 U/ml; normal = 55 to 100 U/ml) due to deficiency of C8 (C8 less than 1,000 CH50 U/ml; normal = greater than or equal to 16,000 CH50 U/ml). This is the first reported case of gonococcal meningitis occurring in a patient with a terminal-complement deficiency. Gonococcal meningitis is a rare complication of gonococcal bacteremia. Both defects in host defenses (e.g., terminal-complement deficiency) and organisms with unusual virulence appear to contribute to the pathogenesis of this complication of gonococcal bacteremia.
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PMID:Comparison of isolates of Neisseria gonorrhoeae causing meningitis and report of gonococcal meningitis in a patient with C8 deficiency. 247 91

Sixty-three Escherichia coli strains isolated from neonatal sepsis or meningitis were studied and compared with previous data on fecal or urinary pyelonephritis-associated isolates from children. Characteristics significantly associated with neonatal infection were capsular type K1 (54%), O group 18 (27%), rough-type lipopolysaccharide together with K1 capsule (19%), and S fimbriae (29%). Within the neonatal infection group, the K1 capsule and rough lipopolysaccharide were most common among the youngest infants (0 to 21 days old) and in meningitis. Hemolysin production, P fimbriae, and X adhesions (adhesions not identifiable as type 1, P, or S) were significantly more common in the two materials from infections as compared with the fecal isolates. One large clone of 11 strains (O18:K1:H7, with both type 1 and S fimbriae) and three smaller ones (O7:K1:H1 and O6:K2:H1, both with type 1 and P fimbriae and X adhesions; and R:K1:H33 with no adhesions) were identified among the strains from neonatal infections. Only O6:K2:H1 strains were also common among the strains from pyelonephritis.
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PMID:Serotypes, hemolysin production, and receptor recognition of Escherichia coli strains associated with neonatal sepsis and meningitis. 258 Jul 92

Serotype b strains of Haemophilus influenzae are strikingly more highly associated with episodes of invasive, life-threatening infection in young children than are strains of other serotypes, but the role that the capsule itself plays in determining this virulence has not been dissected away from that of possibly linked virulence determinants such as lipopolysaccharide (LPS). Using DNA from clinical isolates of all six serotypes (a-f) and a genetically-defined capsule-deficient recipient strain Rb-: 02, we constructed a series of capsular transformants otherwise identical with respect to outer-membrane protein and LPS subtype, biotype, and electrotype. Cloned DNA was also used to create type a and b transformants isogenic outside the capsulation locus to provide the most rigorous test to determine whether capsule alone modulates pathogenicity. Capsular transformants showed the same spectrum of virulence in an infant rat bacteremia/meningitis assay as wild-type strains, thus implicating the capsule polysaccharide as an independent determinant of virulence. Experiments in intact and splenectomised rats identified a critical role for type b capsule in enabling organisms to evade splenic clearance.
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PMID:The molecular basis of pathogenicity in Haemophilus influenzae: comparative virulence of genetically-related capsular transformants and correlation with changes at the capsulation locus cap. 261 36

Intracerebral inoculation of viable Haemophilus somnus resulted in suppurative or fibrino-suppurative meningitis of the brain and spinal cord in rabbits. Multiple fibrin thrombosis complicated with meningitis in the central nervous system was produced by intracerebral inoculation of H. somnus followed by intravenous inoculation with Escherichia coli lipopolysaccharide. The latter reaction may be attributable to a form of Shwartzman reaction.
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PMID:Shwartzman reaction in the brain induced by Haemophilus somnus and Escherichia coli lipopolysaccharide in rabbits. 265 82

Haemophilus influenzae type b (Hib) lipopolysaccharide (LPS) may be present in the cerebrospinal fluid largely as part of outer membrane vesicles (OMV), which could possibly alter its activity. Similar to inoculation of purified Hib LPS, intracisternal inoculation of Hib OMV into adult rats resulted in dose- and time-dependent increases in blood-brain barrier permeability. Polymyxin B, but not an oligosaccharide-specific monoclonal antibody, significantly inhibited the activity of Hib OMV. No change in blood-brain barrier permeability occurred in leukopenic rats inoculated with Hib OMV. Hib OMV was as active as purified Hib LPS on a weight basis and therefore appears to be a relevant vehicle for the delivery of LPS during meningitis.
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PMID:Haemophilus influenzae outer membrane vesicle-induced blood-brain barrier permeability during experimental meningitis. 278 92

It is not clear which factors are responsible for the deficient resistance of human neonates to K1 E. coli sepsis and meningitis. To evaluate the relative importance of different defense mechanisms against bacterial invasion, we have analyzed the sensitivity of newborn mice with known immune deficiencies to infection after oral challenge with virulent K1 E. coli. T and B lymphocyte and complement (C5) defects had no significant effect on natural resistance. In contrast, both endotoxin-hyporesponsive mouse strains tested were highly sensitive. This susceptibility to infection was strongly age dependent. Infant endotoxin-hyporesponsive mice were killed by i.p. injection of less than ten virulent K1 E. coli cells. In contrast, endotoxin-responsive animals and F1 hybrids derived from crosses between endotoxin-responsive and hyporesponsive mice survived an injection with up to 10(4) bacteria. Mutants of a virulent 018:K1 E. coli strain defective in the synthesis of the capsular polysaccharide or the O-antigen of lipopolysaccharide were avirulent as were 01:K1 bacteria, which are under-represented among E. coli isolates from neonatal meningitis. Endotoxin-hyporesponsive mice were protected from lethal bacterial challenge by monoclonal IgG specific for the O-antigen of the challenge strain or by human recombinant interleukin 1. A fulminant bacterial multiplication in the bloodstream of endotoxin-hyporesponsive mice was observed after i.v. injection of 100 virulent K1 E. coli cells. Persistent bacteremia with 10(5) to 10(6) bacteria per ml of blood resulted in death of the animals one to two days after challenge. In the bloodstream of endotoxin-responsive mice the bacteria proliferated to a comparable extent within the first 6 h after challenge. Thereafter they were rapidly cleared from the circulation and the animals recovered from the infection.
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PMID:Host factors in the resistance of newborn mice to K1 Escherichia coli infection. 305 39

Multifocal fibrin thrombosis and suppurative meningitis in the central nervous system was induced by intracerebral inoculation with a cytoplasmic or supernatant fraction of Fusobacterium necrophorum followed by intravenous inoculation with Escherichia coli lipopolysaccharide endotoxin in rabbits. Formation of fibrin thrombosis was reduced by heparin administration. Single intracerebral inoculation with the cytoplasmic or supernatant fraction caused suppurative meningitis. Nervous lesions were often associated with fibrinoid degeneration of the blood vessels. Bacterial lipopolysaccharide endotoxin did not induce apparent meningitis or fibrin thrombosis. The formation of fibrin thrombosis in the central nervous system might be attributable to the Shwartzman reaction.
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PMID:Shwartzman reaction in the brain induced by fractions of Fusobacterium necrophorum and Escherichia coli lipopolysaccharide in rabbits. 306 63

The mechanism(s) by which the lipopolysaccharide (LPS) of Haemophilus influenzae type b may contribute to the virulence of this organism is unclear. Purified LPS of Haemophilus influenzae type b or phosphate buffered saline was administered intranasally to infant rats prior to the intranasal instillation of approximately 2-20 x 10(6) cfu of Hib two or three times per day for three consecutive days. The preadministration of 2.0 micrograms Hib LPS resulted in a significantly greater incidence of bacteremia (P = 0.0006) than PBS 30 min after the completion of the intranasal inoculation. Four days following completion of intranasal Hib inoculation the incidence of bacteremia was greater (P = 0.017) in the animals pretreated with LPS at 2.0 micrograms compared to the PBS pretreated animals. Preadministration of 0.2 micrograms LPS had no effect on the incidence of bacteremia or meningitis. There were no differences in the histology of the nasal cavities or turbinates of infant rats inoculated intranasally only with LPS or PBS. There were no differences in the frequency or density of bacteremia following intranasal administration of LPS from either Hib or E. coli. Although the mechanism is unknown, our findings suggest that the LPS of Hib may contribute to the ability of H. influenzae type b to invade the nasal mucosa in this infant rat model.
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PMID:Contribution of Haemophilus influenzae type b lipopolysaccharide to pathogenesis of infection. 307 63

The percentage of beta-lactamase producing Haemophilus influenzae strains from patients with meningitis in The Netherlands increased from 0% in 1975/1976 to 4.6% in 1985/1986 (n = 1559). Twenty-three isolates resistant to ampicillin, penicillin, chloramphenicol, rifampicin and/or tetracycline were subtyped to determine if one resistant strain was spreading. (Sub)typing was performed by capsular typing, analysis of the major outer membrane protein patterns on sodium dodecylsulfate gels (SDS-PAGE subtypes), lipopolysaccharide serotyping and biotyping. The (sub)types of the resistant strains were similar to those of sensitive strains, thus indicating that antibiotic resistant strains develop at random.
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PMID:Comparison of antibiotic resistant and sensitive strains of Haemophilus influenzae type b in The Netherlands by outer-membrane protein subtyping. 313 38

The factors responsible for blood-brain barrier (BBB) injury during bacterial meningitis are incompletely defined. We evaluated the role of Haemophilus influenzae type b (Hib) lipopolysaccharide (LPS) in the alteration of blood-brain barrier permeability (BBBP) in an adult, normal and leukopenic, rat model of meningitis. Intracisternal inoculation of Hib LPS resulted in (a) dose-dependent increases in BBBP from 2 pg to 20 ng, with significant attenuation in the peak response after challenge with 500 ng and 1 microgram; (b) time-dependent increases in BBBP, with a delayed onset of at least 2 h, maximum alteration at 4 h, and complete reversal at 18 h; (c) greater BBBP than after challenge with the live parent strain; (d) and a close correlation (r = 0.86) between CSF pleocytosis and BBBP at 4 h. The LPS effect was significantly inhibited by preincubation with Polymyxin B and neutrophil acyloxyacyl hydrolase, however two different oligosaccharide-specific monoclonal antibodies did not inhibit activity. No change in BBBP after inoculation with Hib LPS occurred in leukopenic rats. Hib LPS, in the setting of an intact leukocyte response, exerts profound effects on BBBP.
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PMID:Haemophilus influenzae lipopolysaccharide-induced blood brain barrier permeability during experimental meningitis in the rat. 326 27


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