Effect of host lactate on gonococci and meningococci: new concepts on the role of metabolites in pathogenicity.

Abstract

In 1988, Britigan and colleagues (4) showed that the lactate in human neutrophils stimulated oxygen consumption by Neisseria gonorrhoeae and suggested that this might impair their oxygen-dependent bactericidal mechanisms. This first indication that lactate metabolism might be important in the pathogenicity of N. gonorrhoeae has been amply confirmed during the past decade (17, 61, 77), and now lactate has been shown to have important effects on Neisseria meningitidis (15, 16). This review uses the work on gonococci as background to describe recent research on the meningococcus, which in turn provided the key to proving the influence of lactate on gonococcal pathogenicity in vivo. Studies on N. meningitidis showed that, in addition to a general stimulation of metabolism, lactate promotes the production of specific determinants of pathogenicity. Some differences between meningococci and gonococci in their responses to lactate are discussed, and new concepts of the role of metabolites in pathogenicity arising from the work are summarized. Throughout this review, it should be kept in mind that lactate is present in urogenital and respiratory secretions, blood, phagocytes, and cerebrospinal fluid (CSF), together with glucose and pyruvate (61), two other energy sources used effectively by gonococci and meningococci (37, 42, 43). Hence, in vivo, gonococci and meningococci grow on a mixture of carbon sources. To mimic this situation, most of the studies described deal with the influence of lactate on gonococci and meningococci growing in media containing glucose.