Effect of Host Lactate on Gonococci and Meningococci: New Concepts on the Role of Metabolites in Pathogenicity

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Abstract
The original observations of the potential importance of lactate on the behavior of N. gonorrhoeae were reinforced by the demonstration that lactate in blood cell extracts enhanced the sialylation of gonococcal lipopolysaccharide (LPS) by cytidine-5′-monophospho-N-acetyl neuraminic acid (CMP-NANA) (49). Previous observations of gonococci harvested from urethral exudates had shown that host-derived CMP-NANA was incorporated into their LPS, rendering them resistant to killing by complement-mediated lysis in human serum, by phagocytes, and by antibody (24, 60). The enhancing effect of physiological concentrations of lactate on LPS sialylation occurred as gonococci were emerging from lag phase in a medium containing glucose. This resulted from an overall stimulation of metabolism, evidenced by greater LPS production (by 10 to 20%), enhanced protein synthesis (10 to 20%), and larger pentose contents (30 to 60%) (21, 22). Increased LPS sialylation occurs through greater production of both LPS and the sialyltransferase. There was more rapid emergence from lag phase with lactate and a 20% increase in the rate of logarithmic growth compared with glucose alone (22). Lactate was used more rapidly than glucose in a synthetic medium (22), as was seen in the fluid obtained from subcutaneous plastic chambers in guinea pigs that had been infected with gonococci (25).

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