1887

Abstract

The synthesis of cell-associated and secreted proteins by FSS2, an infective endocarditis (IE) isolate, was influenced by both environmental pH and carbon source. Controlling the pH at 75 in stirred batch cultures showed that cell-associated and secreted protein concentrations were increased during late exponential and stationary phase by 68% and 125%, respectively, compared with similar cultures without pH control. The expression of five glycosidase and eight peptidase activities were examined using fluorogen-labelled synthetic substrates. Enzyme activities were significantly down-regulated during exponential growth, increasing during stationary phase (<001) whether the culture pH was controlled at pH 75 or allowed to fall naturally to pH 44. Culture-supernatant activities were significantly increased (<005) when the pH was maintained at 60 or 75, indicating modulation of enzyme activity by pH. Growth under nitrogen-limitation/glucose-excess conditions resulted in a significant repression of cell-associated glycosidase activities (<001), whilst in the supernatant, activities were generally reduced. The expression of peptidase activities in the culture supernatant did not significantly change. The results suggest a possible role for catabolite repression by glucose in regulating enzyme expression. When FSS2 was cultured with 50% (v/v) added heat-inactivated foetal bovine serum, several cell-associated enzyme activities increased initially but were then reduced as the culture time was extended to 116 h. Culture-supernatant enzyme activities (-acetyl-β-D-glucosaminidase, -acetyl-β-D-galactosaminidase, thrombin, Hageman factor, collagenase and chymotrypsin), however, were significantly increased (<001) over the same time period. The findings indicated that most of the important glycosidases synthesized by FSS2 were down-regulated by acid growth conditions and may also be subject to catabolite repression by glucose but conversely may be up-regulated by growth in serum. These results may have implications for streptococcal growth in an IE vegetation and in the mouth between meals or during sleep.

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2000-08-01
2019-12-11
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References

  1. Beighton, D., Homer, K. A. & Kelley, S. ( 1995; ). The production of protease activities by Streptococcus oralis strains isolated from endocarditis. Microb Ecol Health Dis 8, 213-218.[CrossRef]
    [Google Scholar]
  2. Durack, D. T. & Beeson, P. B. ( 1972; ). Experimental bacterial endocarditis. II. Survival of bacteria in endocarditis vegetations. Br J Exp Pathol 53, 50-53.
    [Google Scholar]
  3. Ferguson, D. L., McColm, A. A., Ryan, D. M. & Acred, P. ( 1986; ). A morphological study of experimental staphylococcal endocarditis and aortitis. II. Inter-relationship of bacteria, vegetation and cardiovasculature in established infections. Br J Exp Pathol 67, 679-686.
    [Google Scholar]
  4. Ford, I. & Douglas, C. W. I. ( 1997; ). The role of platelets in infective endocarditis. Platelets 8, 285-294.[CrossRef]
    [Google Scholar]
  5. Herzberg, M. C. ( 1996; ). Platelet–streptococcal interactions in endocarditis. Crit Rev Oral Biol Med 7, 222-236.[CrossRef]
    [Google Scholar]
  6. Herzberg, M. C. & Meyer, M. W. ( 1996; ). Effects of oral flora on platelets: possible consequences in cardiovascular disease. J Periodontol 67, 1138-1142.[CrossRef]
    [Google Scholar]
  7. Herzberg, M. C., MacFarlane, G. D., Ke Gong, Armstrong, N. N., Witt, A. R., Erickson, P. R. & Meyer, M. W. ( 1992; ). The platelet interactivity phenotype of Streptococcus sanguis influences the course of experimental endocarditis. Infect Immun 60, 4809–4818.
    [Google Scholar]
  8. Homer, K. A., Kelley, S., Hawkes, J., Beighton, D. & Grootveld, M. C. ( 1996; ). Metabolism of glycoprotein-derived sialic acid and N-acetylglucosamine by Streptococcus oralis. Microbiology 142, 1221-1230.[CrossRef]
    [Google Scholar]
  9. Ke Gong, Ouyang, T. & Herzberg, M. C. ( 1998; ). A streptococcal adhesion system for salivary pellicle and platelets. Infect Immun 66, 5388–5392.
    [Google Scholar]
  10. Laemmli, U. K. ( 1970; ). Cleavage of structural proteins during the assembly of the head of bacteriophage T4. Nature 227, 680-685.[CrossRef]
    [Google Scholar]
  11. Lowrance, J. H., Hasty, D. L. & Simpson, W. A. ( 1988; ). Adherence of Streptococcus sanguis to conformationally specific determinants in fibronectin. Infect Immun 56, 2279-2285.
    [Google Scholar]
  12. Manning, J. E., Geylin, A. J., Ansmits, L. M., Oakey, H. J. & Knox, K. W. ( 1994a; ). A comparative study of the aggregation of human, rat and rabbit platelets by members of the Streptococcus sanguis group. J Med Microbiol 41, 10-13.[CrossRef]
    [Google Scholar]
  13. Manning, J. E., Hume, E. B. H., Hunter, N. & Knox, K. W. ( 1994b; ). An appraisal of the virulence factors associated with streptococcal endocarditis. J Med Microbiol 40, 110-114.[CrossRef]
    [Google Scholar]
  14. Marrie, T. J., Cooper, M. B. & Costerton, J. B. ( 1987; ). Ultrastructure of cardiac bacterial vegetations on native valves with emphasis on alterations in bacterial morphology following antibiotic treatment. Can J Cardiol 3, 275-280.
    [Google Scholar]
  15. Mayo, J. A., Zhu, H., Harty, D. W. S. & Knox, K. W. ( 1995; ). Modulation of glycosidase and protease activities by chemostat growth conditions in an endocarditis strain of Streptococcus sanguis. Oral Microbiol Immunol 10, 342-348.[CrossRef]
    [Google Scholar]
  16. Meyer, M. W., Ke Gong & Herzberg, M. C. ( 1998; ). Streptococcus sanguis-induced platelet clotting in rabbits and hemodynamic and cardiopulmonary consequences. Infect Immun 66, 5906–5914.
    [Google Scholar]
  17. Mills, J., Pulliam, L., Dall, L., Marzouk, J., Wilson, W. & Costerton, J. W. ( 1984; ). Exopolysaccharide production by viridans streptococci in experimental endocarditis. Infect Immun 43, 359-367.
    [Google Scholar]
  18. Oakey, H. J., Harty, D. W. S. & Knox, K. W. ( 1995; ). Enzyme production by lactobacilli and the potential link with infective endocarditis. J Appl Bacteriol 78, 142-148.[CrossRef]
    [Google Scholar]
  19. Pitty, L. J. & Jacques, N. A. ( 1989; ). Dissimilar effects of Na+ and K+ on the promotion of glucosyltransferase secretion in Streptococcus salivarius. J Gen Microbiol 135, 1431-1439.
    [Google Scholar]
  20. Rafay, A. M., Homer, K. A. & Beighton, D. ( 1996; ). Effect of mucin and glucose on proteolytic and glycosidic activities of Streptococcus oralis. J Med Microbiol 44, 409-417.[CrossRef]
    [Google Scholar]
  21. Terleckyj, B., Willet, N. P. & Shockman, G. D. ( 1975; ). Growth of several cariogenic strains of oral streptococci in a chemically-defined medium. Infect Immun 11, 649-655.
    [Google Scholar]
  22. Vriesema, A. J. M., Dankert, J. & Zaat, S. A. J. ( 2000; ). A shift from oral to blood pH is a stimulus for adaptive gene expression of Streptococcus gordonii CH1 and induces protection against oxidative stress and enhanced bacterial growth by expression of msrA. Infect Immun 68, 1061-1068.[CrossRef]
    [Google Scholar]
  23. Whiley, R. A. & Beighton, D. ( 1998; ). Current classification of the oral streptococci. Oral Microbiol Immunol 13, 195-216.[CrossRef]
    [Google Scholar]
  24. Wittenberger, C. L., Beaman, A. J. & Lee, L. N. ( 1978; ). Tween 80 effect on glucosyltransferase synthesis by Streptococcus salivarius. J Bacteriol 133, 231-239.
    [Google Scholar]
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