Evidence that glucose and sucrose uptake in oral streptococcal bacteria involves independent phosphotransferase and proton-motive force-mediated mechanisms.
Sugar transport and glycolysis in Streptococcus sanguis NCTC 7865, Streptococcus mitis ATCC 903, Streptococcus salivarius NCTC 8606 and several strains of Streptococcus mutans were investigated by following the rate of acid production by washed bacteria at a constant pH of 7.0. The phosphoenolpyruvate-phosphotransferase system (PTS) was inhibited by low concentrations of chlorhexidine. When this PTS-inhibitory concentration of chlorhexidine was added to cells washed and re-suspended in KCl, glucose uptake and glycolysis continued at a greatly-reduced rate. Chlorhexidine abolished glucose and sucrose uptake and metabolism in bacteria washed and incubated in saline. The Na+-inhibition was reproduced in KCl-washed bacteria using the cyclic peptide ionophores, valinomycin and gramicidin, to dissipate K+ and H+ gradients across the cell membrane. Glucose metabolism by Strep. mutans B13 was more resistant to chlorhexidine than that of Strep. mutans NCTC 10449 or Strep. sanguis but was more sensitive to the ionophores. Valinomycin had a greater inhibitory effect on strain B13 than the other two. That ion gradients are important in the chlorhexidine-resistant glucose-uptake mechanism was confirmed using the classical uncoupling agents, carbonylcyanide-m-chlorophenylhydrazone, 2,4-dinitrophenol and KSCN. Glucose metabolism was inhibited in the presence of both the uncouplers and the PTS-inhibitory concentration of chlorhexidine and significant inhibition was also observed in the absence of the PTS inhibitor. Lactate or the ATPase inhibitor, dicyclohexyl carbodiimide (DCCD), had similar inhibitory effects on the non-PTS uptake system.(ABSTRACT TRUNCATED AT 250 WORDS)
D000251:Adenosine Triphosphatases / Q000378:metabolism; D001693:Biological Transport, Active / Q000187:drug effects; D002710:Chlorhexidine / Q000494:pharmacology; D004563:Electrochemistry; D005947:Glucose / Q000378:metabolism*; D006019:Glycolysis / Q000187:drug effects; D006801:Humans; D007476:Ionophores / Q000494:pharmacology; D007773:Lactates / Q000037:antagonists & inhibitors; D009055:Mouth / Q000382:microbiology*; D010770:Phosphotransferases / Q000378:metabolism*; D011522:Protons; D012964:Sodium / Q000494:pharmacology; D013291:Streptococcus / Q000187:drug effects / Q000378:metabolism*; D013395:Sucrose / Q000378:metabolism*; D014475:Uncoupling Agents / Q000494:pharmacology
D007476:Ionophores; D007773:Lactates; D011522:Protons; D014475:Uncoupling Agents; D013395:Sucrose; D012964:Sodium; D010770:Phosphotransferases; D000251:Adenosine Triphosphatases; D005947:Glucose; D002710:Chlorhexidine