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)

Despite the availability of effective antimicrobial agents and aggressive public health programmes, gonococcal infections, including salpingitis, remain a major worldwide problem resulting in significant rates of morbidity and infertility. Using an experimental model of gonococcal-infected human fallopian tubes in organ culture which are examined by light microscopy and scanning and transmission electron microscopy, basic pathogenic interactions between the gonococcus and the fallopian tube have been elucidated. The major steps in the pathogenic process include attachment, damage and invasion. Attachment appears to result from interaction of gonococcal pili with the tips of microvilli of non-ciliated cells of the fallopian tube mucosa. After gonococcal attachment occurs, fallopian tube damage is evident with loss of ciliary activity and sloughing of ciliated cells. The 2 compounds most likely to be mediators of this damage appear to be gonococcal lipopolysaccharide, which is released from the surface of the organism in the form of outer membrane blebs, as well as monomeric units of peptidoglycan, which are elaborated by the organism. Gonococcal attachment and perhaps elaboration of some molecule appear to initiate phagocytosis by non-ciliated epithelial cells. Gonococci are transported to the base of the non-ciliated cells and are released into the subepithelial space. This may lead to local disease (salpingitis) or disseminated disease (dermatitis-arthritis). Understanding the molecular mechanisms by which gonococci attach to, damage or invade the fallopian tube mucosa may result in identification of ways of preventing gonococcal infections and their sequelae.
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PMID:Molecular mechanisms of pathogenicity of gonococcal salpingitis. 287 17

Studies of the interaction between Neisseria gonorrhoeae and human fallopian tube mucosa in organ culture suggest that attachment of gonococci is important, not only to secure th organism in the host, but also to initiate the disease process. The steps observed in gonococcal infection of fallopian tube organ cultures are: 1) attachment of gonococci to microvilli of nonciliated cells; 2) release from gonococci of lipopolysaccharide and possibly other toxic moities to cause mucosa damage; 3) engulfment or phagocytosis of gonococci by nonciliated cells; 4) transport of phagocytic vacuoles containing gonococci to the base of the nonciliated cells; and 5) exocytosis of gonococci within phagocytic vacuoles into the subepithelial tissues. In vivo, these steps might result in extensive local disease (e.g. salpingitis) or in the invasion of blood vessels to cause disseminated disease. Preliminary studies of human nasopharyngeal tissue in organ culture infected with Neisseria meningitidis indicate that meningococci attach to microvilli of nonciliated cells and are phagocytized by these cells. Meningococci subsequently appear in subepithelial tissues, though the route they take is not yet certain. These observations suggest at least some of the ways in which attachment may play a role in disease caused by N. gonorrhoeae and N. meningitidis. Mechanisms to block this attachment may provide new approaches to the prevention of infections caused by the pathogenic Neisseria.
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PMID:Attachment of pathogenic Neisseria to human mucosal surfaces: role in pathogenesis. 612 78

Principal outer membrane protein (protein I) of Neisseria gonorrhoeae was prepared nearly free of lipopolysaccharide (LPS) and substantially purified from other membrane proteins by chromatography of partially purified gonococcal outer membranes over Sepharose 6B in the presence of deoxycholate at pH 9.0. This protein I of nine separate antigenic types was coated to polystyrene tubes and used in the enzyme-linked immunosorbent assay (ELISA) to measure antibody to protein I or in inhibition tests to quantitate protein I antigen. No significant inhibition of the ELISA test was produced by purified LPS from the strain used to prepare each of the protein I types or by whole gonococci bearing the same LPS but different protein I antigens as the strain used to produce a given protein I antigen. Of 125 strains of gonococci used as whole organisms to inhibit the protein I ELISA, 124 (99%) typed with one or more of the nine protein I types, and 35% of these typed with a single protein I serotype. Sixty-one of 65 (94%) strains from Seattle and Atlanta patients with disseminated gonococcal infection contained protein I serotype 1, and 16 of 24 (64%) strains from Seattle patients with salpingitis bore one or both of protein I serotypes 1 and 2.
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PMID:Antigen-specific serotyping of Neisseria gonorrhoeae: characterization based upon principal outer membrane protein. 616 68

Gonococci damaged the mucosa of human fallopian tubes in organ culture (FTOC), producing characteristic pathologic features. Filter-sterilized supernatant fluid from donor gonococcal-infected FTOC damaged recipient FTOC in a similar fashion. Gonococcal lipopolysaccharide (LPS) was detected in these toxic donor fluids in concentrations of 1.2 to 8.3 microgram/ml. Purified gonococcal LPS in concentrations as low as 0.015 microgram/ml produced damage equivalent to that caused by toxic donor fluid and was neutralized by polymyxin B. Such LPS-mediated damage to ciliated cells, if it occurs in gonococcal salpingitis, may impair mucociliary flow and predispose to ectopic pregnancy and recurrent ascending infection.
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PMID:Gonococcal lipopolysaccharide: a toxin for human fallopian tube mucosa. 678 51

A Swiss Webster white mouse model of salpingitis was used to characterize the immune response following an intrauterine infection with the Chlamydia trachomatis mouse pneumonitis biovar. Western blot (immunoblot) analyses of the serum samples showed that the immunodominant bands corresponded to molecular masses of 72, 60, 42, and 28 kDa and to the lipopolysaccharide. Antibodies to the 60-kDa heat shock protein and to the 60-kDa cysteine-rich protein were detected at 2 and 3 weeks postinfection, respectively. Neutralization was observed in an in vitro assay with serum samples as early as the 3rd day postinfection and remained high for the 7 weeks of observation. The mice were mated in the 7th week following infection. Of the infected experimental mice, 71.4% were found to be either unilaterally or bilaterally infertile, whereas only 27.4% of the noninfected control mice were found to be infertile.
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PMID:Analysis of the immune response in mice following intrauterine infection with the Chlamydia trachomatis mouse pneumonitis biovar. 842 4