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Mutagenesis of the Neisseria gonorrhoeae porin reduces invasion in epithelial cells and enhances phagocyte responsiveness
Author(s) -
Bauer Frank J.,
Rudel Thomas,
Stein Markus,
Meyer Thomas F.
Publication year - 1999
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1046/j.1365-2958.1999.01230.x
Subject(s) - porin , biology , neisseria gonorrhoeae , mutant , bacterial outer membrane , microbiology and biotechnology , mutagenesis , gene , genetics , escherichia coli
Porin (PorB), the major outer membrane protein of Neisseria gonorrhoeae , has been implicated in pathogenesis previously. However, the fact that porin deletion mutants are not viable has complicated investigations. Here, we describe a method of manipulating the porin gene site‐specifically. N. gonorrhoeae MS11, which harbours the porB 1B (P.1B) porin allele, was used to generate mutants carrying deletions in the surface loops 1 and 5. An 11‐amino‐acid deletion in loop 1 impaired Opa 50 ‐dependent invasion into human Chang epithelial cells, whereas loop 5 deletion exhibited no apparent phenotype. In a second approach, the complete gonococcal porB 1B was replaced by the porB Nla gene of Neisseria lactamica . Such mutants were unable to induce efficient uptake by epithelial cells but induced an enhanced respiratory response in HL60 phagocytic cells. The increased respiratory burst was accompanied by an enhanced phagocytic uptake of the mutant compared with the wild‐type strain. Our data extend previous evidence for multiple central functions of PorB in the infection process.