| pubmed-article:7553571 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:7553571 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:7553571 | lifeskim:mentions | umls-concept:C0027571 | lld:lifeskim |
| pubmed-article:7553571 | lifeskim:mentions | umls-concept:C1704675 | lld:lifeskim |
| pubmed-article:7553571 | lifeskim:mentions | umls-concept:C0450254 | lld:lifeskim |
| pubmed-article:7553571 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:7553571 | pubmed:dateCreated | 1995-10-25 | lld:pubmed |
| pubmed-article:7553571 | pubmed:abstractText | The ability to interact with nonphagocytic cells is a crucial virulence attribute of the meningococcus and the genococcus. Like most bacterial pathogens, Neisseria meningitidis and Neisseria gonorrhoeae initiate infections by colonizing the mucosal epithelium, which serves as the site of entry. After this step, both bacteria cross the intact mucosal barrier. While N. gonorrhoeae is likely to remain in the subepithelial matrix, where it initiates an intense inflammatory reaction, N. meningitidis enters the bloodstream, and eventually the cerebrospinal fluid to cause meningitis. Both pathogens have evolved very similar mechanisms for interacting with host cells. Surface structures that influence bacterium-host interactions include pili, the meningococcal class 5 outer membrane proteins or the gonococcal opacity proteins, lipooligosaccharide, and the meningococcal capsule. This review examines what is known about the roles these structures play in bacterial adhesion and invasion, with special emphasis, on pilus-mediated adhesion. Finally, the importance of these structures in neisserial pathogenesis is discussed. | lld:pubmed |
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