Attachment of pathogenic Neisseria to human mucosal surfaces: Role in pathogenesis

D. S. Stephens, Z. A. McGee, M. Ann Melly, C. R. Gregg, L. H. Hoffman

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Abstract

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 the 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.

Original languageEnglish (US)
Pages (from-to)192-195
Number of pages4
JournalInfection
Volume10
Issue number3
DOIs
StatePublished - May 1 1982

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ASJC Scopus subject areas

  • Microbiology (medical)
  • Infectious Diseases

Cite this

Stephens, D. S., McGee, Z. A., Ann Melly, M., Gregg, C. R., & Hoffman, L. H. (1982). Attachment of pathogenic Neisseria to human mucosal surfaces: Role in pathogenesis. Infection, 10(3), 192-195. https://doi.org/10.1007/BF01640777