Abstract
In this issue of the Journal of Bacteriology, Olesky et al. (13) report a novel observation regarding the mechanism by which Neisseria gonorrhoeae developed clinically significant levels of resistance to penicillin. Although yet to be fully defined, their results link changes in the structure of a gonococcal porin (PorB), which was presumed to modulate permeation of penicillin due to precedents set by studies with porins from Enterobacteriaceae (1, 11), with overexpression of a multidrug efflux pump and the development of penicillin resistance in gonococci. The implications of their work for further advancing our knowledge regarding the structure-function relationships of the gram-negative cell envelope, differences between such bacteria in this respect, and the connection of efflux pumps with other cell envelope proteins in the development of antibiotic resistance are substantial. Moreover, the findings justify continued research on basic problems of antibiotic resistance even when the antibiotic in question is no longer used clinically to treat the disease in question.
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