Molecular mechanisms of pathogenicity of gonococcal salpingitis.
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.
Woods
M L
ML
McGee
Z A
ZA
D000268:Adhesiveness; D002923:Cilia / Q000502:physiology; D005187:Fallopian Tubes / Q000382:microbiology* / Q000502:physiology; D005260:Female; D010861:Fimbriae, Bacterial / Q000502:physiology; D006069:Gonorrhea / Q000382:microbiology*; D006801:Humans; D008070:Lipopolysaccharides / Q000502:physiology; D008871:Microvilli / Q000378:metabolism; D009092:Mucous Membrane / Q000382:microbiology; D009344:Neisseria gonorrhoeae / Q000502:physiology*; D010457:Peptidoglycan / Q000502:physiology; D012488:Salpingitis / Q000382:microbiology*
D008070:Lipopolysaccharides; D010457:Peptidoglycan