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

The virulence of lipopolysaccharide (LPS) variants of Neisseria gonorrhoeae strain Gc40 was studied in vivo using the guinea-pig subcutaneous chamber model. Survival of variants D1, D2, D4 and D5 was assessed by viable counts made on chamber fluid at various times after inoculation. Chemotactic effect was measured by counts of white cells in the chambers. Differential cell counts and assessments of the location of the gonococci were made on Giemsa-stained smears of chamber fluid. Sensitivity of the variants to normal guinea-pig serum was determined by in vitro bactericidal assays. D1 and D5 had relatively high Mr LPS which was shed in the medium, were serum resistant, produced intense infections and were mainly extracellular. Large number of damaged white cells were present. D2 and D4, had low Mr LPS which was poorly shed in the medium, were serum sensitive and produced low grade infections. D2 was the least infective and was seen mainly inside neutrophils. Collectively the data indicates that the type of LPS on the gonococcal surface and possibly the amount of shed LPS strongly influence the fate of gonococci in vivo, in an environment in which antibodies, complement and phagocytic cells are freely available. This may be decisive at some stages of the human infection.
 ...
PMID:Alterations of the LPS determine virulence of Neisseria gonorrhoeae in guinea-pig subcutaneous chambers. 180 Aug 89

Gonococci examined directly from urethral exudates are resistant to killing by human serum, but most strains become susceptible on subculture. Previous work with gonococci grown in vitro indicates that resistance in vivo is due to sialylation of gonococcal lipopolysaccharide (LPS) by a host factor, cytidine 5'-monophospho-N-acetylneuraminic acid (CMP-NANA) or a related compound present in urogenital secretions and blood cells including phagocytes, which exude during inflammation. This sialylation inhibits the reaction between bactericidal IgM in serum and its target LPS sites. Here, we confirm the indication by using gonococci grown in vivo. Crucial to the above conclusions was the marked reduction of CMP-NANA-conferred serum resistance when gonococci were treated with neuraminidase to remove sialyl groups from their LPS. We now show that the serum resistance of gonococci in urethral exudates was reduced by treatment with neuraminidase from more than 95% (calculated in relation to controls incubated with heated serum) to 2-11% according to sample and incubation time. Subculture of the gonococci also reduced resistance to 9-11% but resistance was restored to more than 95% by incubation with CMP-NANA. This work is the culmination of an investigation that underlines the need to identify specific host factors and the virulence determinants they induce in vivo in future studies of pathogenicity.
 ...
PMID:Resistance to human serum of gonococci in urethral exudates is reduced by neuraminidase. 197 33

A plasmid, pTME6, containing Neisseria gonorrhoeae lipopolysaccharide biosynthesis genes was used as a probe to analyze DNA from strains of N. gonorrhoeae, N. meningitidis and various commensal Neisseria by Southern blotting. Chromosomal DNA from 26 gonococcal strains probed with 32P-labeled pTME6 produced five different hybridization patterns. No correlation between hybridization pattern and auxotype, serotype, serum sensitivity or SDS-urea-PAGE migration of LPS was observed. DNA from strains of N. meningitidis, N. lactamica and N. cinerea, but not other commensal Neisseria species, hybridized strongly to pTME6.
 ...
PMID:Distribution of gonococcal lipopolysaccharide biosynthesis genes among strains of Neisseria gonorrhoeae and other neisserial species. 211 67

Gonococci do not cause genital infection in any convenient experimental animal, but all too easily cause genital infection in humans. To determine the 'evolutionary watershed' of gonococcal infections (the point on the evolutionary tree at which susceptibility to gonococcal infection begins) we extended previous studies of the interaction of gonococci with animal oviduct mucosa to include chimpanzees and baboons. Gonococci attached to, damaged, and invaded the oviduct (fallopian tube) mucosa of chimpanzees (which are apes) but not the oviduct mucosa of baboons (which are monkeys). Thus, the pattern of gonococcal infection in chimpanzees was identical to that in humans, whereas the pattern in baboons was like that in other animals. These studies indicate that the point in evolution at which susceptibility to gonococcal infection commences is between baboons and chimpanzees (or between monkeys and apes). Susceptibility to gonococcal disease appears to require the presence on genital epithelial cells of receptors for gonococcal ligands such as pili, receptors for gonococcal lipopolysaccharide, or both. The physiological role of these receptors may be to interact with more useful, as yet unidentified molecules.
 ...
PMID:The evolutionary watershed of susceptibility to gonococcal infection. 212 57

Resistance to normal human serum (NHS) killing in Neisseria gonorrhoeae has been associated with particular types of Protein I (PI) and lipopolysaccharide (LPS), but many exceptions exist, and the role of these structures in determining serum reactivities remains controversial. In reality, the response of the gonococcus to NHS is probably governed by several parameters involving a number of outer-membrane (OM) components. We surveyed the serum reactivities of 14 strains of N. gonorrhoeae and characterized each of their major OM components. The strains presented a spectrum of sensitivity to pooled NHS. As assessed by sodium dodecyl sulphate-polyacrylamide gel electrophoresis, immunoblotting, and peptide mapping, the strains were also quite heterogeneous in terms of PI, H.8 antigen, and LPS type, and the presence of the 2-1-L8 epitope. Five of the strains had identical PIAs in varying LPS and H.8 backgrounds, and four had identical PIBs in varying LPS and H.8 backgrounds. As assessed by electrophoretic migration and monoclonal antibody binding, Protein III and the 44,000 Dalton protein were identical in these strains. We found no association between PI subclass and serum sensitivity, while H.8 and LPS variation appeared to be related to bactericidal responses. The diversity and close interaction of gonococcal components in the OM are undoubtedly involved in differential abilities to survive NHS killing.
 ...
PMID:Characterization of fourteen strains of Neisseria gonorrhoeae: structural analyses and serum reactivities. 212 25

The determinant(s) of gonococcal resistance to killing by human phagocytes has been extracted from outer membrane vesicles (OMV) of a phagocyte-resistant strain, BS4 (agar), with sodium cholate (1%, w/v). The extracts, like the OMV, nullified the effect of antiserum raised against whole BS4 (agar) to promote intracellular killing of the latter by human peripheral blood phagocytes. Fractionation of the extract on Sephadex G75 produced an active fraction with much less protein and lipopolysaccharide (LPS) than in the original extract. Furthermore, crude LPS prepared from the resistant gonococci was inactive. These results imply that the factor(s) promoting intracellular resistance is a protein. SDS-PAGE of the active fraction suggested that the factor was not a principal outer membrane protein nor one of three proteins previously thought to be associated with resistance. In contrast to a similar preparation from a phagocyte-susceptible strain, BSSH, the active fraction from BS4 (agar) showed faintly staining proteins in the regions of 20 and 60 kDal. When eluted from the gels, the former but not the latter neutralized the above effect of antisera, thus associating the 20 kDal protein(s) with resistance to intracellular killing.
 ...
PMID:Association of resistance of Neisseria gonorrhoeae to killing by human phagocytes with outer-membrane proteins of about 20 kilodaltons. 241 May 44

This study was done to define antigens important in the immune response to infection with Neisseria gonorrhoeae. Sera were obtained from men and women with uncomplicated gonorrhea (UGC), women with disseminated gonococcal infection, and women with gonococcal pelvic inflammatory disease (PID); sera were also obtained from uninfected controls. Vaginal fluids were taken from 15 patients with UCG or PID. The sera and vaginal fluids were tested against gonococcal isolates from the same patients to examine homologous antibody-antigen interactions by use of the western blot technique. Antibodies in the serum reacted with more gonococcal antigens compared with antibodies in the vaginal fluid. IgG in serum and vaginal fluid reacted with more antigens than did IgA in the same specimens. The predominant antigens reactive with IgG in serum were pili, protein II, a broad 23-33-kDa band of antigen, and presumptive lipopolysaccharide; and for IgA, protein II and a 46-48-kDa protein. The control sera also reacted with the 46-48-kDa protein. The predominant antigens reactive with IgG in vaginal fluid were protein I, protein II, pili, and the 46-48-kDa protein; and for IgA, protein I, protein II, and pili. Immunoglobulin in vaginal fluid reacted comparatively more with protein I than did immunoglobulin in serum.
 ...
PMID:Antibody-antigen specificity in the immune response to infection with Neisseria gonorrhoeae. 241 48

An experimental model using human fallopian tubes in organ culture was used to study the localization of purified gonococcal lipopolysaccharide (LPS). LPS was visualized by light microscopy with immunoperoxidase staining. Immediately after addition to fallopian tube organ cultures, gonococcal LPS aggregated on the tips of cilia. By 1 to 2 h after exposure, LPS could be seen distributed throughout the cytoplasm of ciliated and nonciliated cells in structures resembling vesicles. By 12 h, there were sloughed, ciliated cells present in the fallopian tube lumen, which had positive LPS stain on their surfaces as well as in their cytoplasm. By 24 h, LPS was distributed throughout the cytoplasm. Control experiments with rabbit oviduct organ cultures showed that LPS failed to attach, enter, or damage mucosal cells. These studies illustrate the initial localization of LPS on human mucosal cells and its uptake into the cells, which are coincident with toxicity for ciliated epithelial cells.
 ...
PMID:Localization of gonococcal lipopolysaccharide and its relationship to toxic damage in human fallopian tube mucosa. 241 54

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.
 ...
PMID:Comparison of isolates of Neisseria gonorrhoeae causing meningitis and report of gonococcal meningitis in a patient with C8 deficiency. 247 91

Nonbactericidal monoclonal antibodies (MAbs) directed against gonococcal surface antigens were examined for their effect on complement-mediated bactericidal killing by other MAbs and normal human serum. One MAb, SM73, directed against the H.8 antigen activated complement only moderately well and had little influence on bactericidal antibodies. Two antibodies directed against an epitope on protein III had very different effects. Antibody SM51 activated complement poorly and had no effect on bactericidal killing, whereas antibody SM50, although itself nonbactericidal, activated complement and blocked the bactericidal effect of other antibodies. The extent of the blocking ability of MAb SM50 was studied using MAbs of different specificities as well as polyclonal antisera raised against gonococcal surface antigens. Antibody SM50 blocked IgG MAbs of all specificities, but several MAbs of the IgM class retained their bactericidal effect. Each of these IgM MAbs reacted with lipopolysaccharide, but with different epitopes.
 ...
PMID:Nonbactericidal antibodies against Neisseria gonorrhoeae: evaluation of their blocking effect on bactericidal antibodies directed against outer membrane antigens. 247 27


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>