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Phase variation of lipopolysaccharide directs interconversion of invasive and immuno‐resistant phenotypes of Neisseria gonorrhoeae.
Author(s) -
Putten J.P.
Publication year - 1993
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1002/j.1460-2075.1993.tb06088.x
Subject(s) - phase variation , neisseria gonorrhoeae , biology , microbiology and biotechnology , lipopolysaccharide , complement system , sialic acid , antibody , classical complement pathway , phenotype , glycoprotein , n acetylneuraminic acid , immune system , neisseria meningitidis , antigenic variation , alternative complement pathway , bacteria , immunology , gene , genetics
Phase variation of Neisseria gonorrhoeae lipopolysaccharide (LPS) controls both bacterial entry into human mucosal cells, and bacterial susceptibility to killing by antibodies and complement. The basis for this function is a differential sialylation of the variable oligosaccharide moiety of the LPS. LPS variants that incorporate low amounts of sialic acid enter human mucosal epithelial cells very efficiently, but are susceptible to complement‐mediated killing. Phase transition to a highly sialylated LPS phenotype results in equally adhesive but entry deficient bacteria which, however, resist killing by antibodies and complement because of dysfunctional complement activation. Phase variation of N. gonorrhoeae LPS thus functions as an adaptive mechanism enabling bacterial translocation across the mucosal barrier, and, at a later stage of infection, escape from the host immune defence.