Abstract

Streptococcus gordonii is an etiological bacterial agent of infective endocarditis. Although the pathogenesis mechanisms are not well understood, the interaction between streptococci and phagocytes is considered important for the development of infective endocarditis. Previous studies show that some S. gordonii strains, including DL1, survive in polymorphonuclear leukocytes (PMNs), whereas other strains such as SK12 are sensitive to PMN-dependent killing. In this study, we assessed the differences between the sensitivity of S. gordonii DL1 and S. gordonii SK12 to PMN-dependent killing. S. gordonii DL1 showed a higher survival when treated with PMNs than SK12. Both S. gordonii DL1 and S. gordonii SK12 showed high resistance to low pH condition. Compared to S. gordonii SK12, S. gordonii DL1 was sensitive to hydrogen peroxide. However, the resistance of S. gordonii DL1 to the tested bactericidal agents, especially lysozyme, was higher than that of SK12. Furthermore, we performed a bactericidal assay by treating a mixture of S. gordonii DL1 and SK12 with PMNs. S. gordonii DL1 did not enhance the survival of S. gordonii SK12 exposed to PMNs. These results indicated that S. gordonii DL1 is resistant to bactericidal agents that degrade bacteria in phagolysosomes. In addition, there was no secretory factor involved in the resistance to bactericidal agents. The findings of this study may help develop treatments for infective endocarditis caused by S. gordonii.

Highlights

  • We first investigated the survival of S. gordonii DL1 and SK12 treated with polymorphonuclear leukocytes (PMNs)

  • These data suggest that the sensitivity of S. gordonii SK12 to PMN-dependent killing was higher than that of S. gordonii DL1

  • Lee et al revealed that pathogenic S. gordonii strains are resistant to PMN-dependent killing, whereas a large number of non-pathogenic S. gordonii strains are killed by PMNs [17]

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Summary

Objectives

The aim of this study was to determine the potential mechanisms associated with the differences in resistance between S. gordonii DL1 and SK12 to PMN-mediated killing, and determine the potential mechanisms associated with resistance

Methods
Results
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