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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Front+Cell+Infect+Microbiol
2017 ; 7
(ä): 97
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A Nuclease from Streptococcus mutans Facilitates Biofilm Dispersal and Escape
from Killing by Neutrophil Extracellular Traps
#MMPMID28401067
Liu J
; Sun L
; Liu W
; Guo L
; Liu Z
; Wei X
; Ling J
Front Cell Infect Microbiol
2017[]; 7
(ä): 97
PMID28401067
show ga
Streptococcus mutans is the primary etiologic agent of dental caries and
occasionally infective endocarditis, with the ability to form biofilms and
disperse cells into distal sites to exacerbate and spread infection. In this
study, we identified a nuclease (DeoC) as a S. mutans biofilm dispersal
modulating factor through microarray analysis. In vitro assays revealed a
dispersal defect of a deoC deletion mutant, and functional studies with purified
protein were indicative of the biofilm dispersal activity of DeoC. Neutrophils
are a key host response factor restraining bacterial spreading through the
formation of neutrophil extracellular traps (NETs), which consist of a nuclear
DNA backbone associated with antimicrobial peptides. Therefore, we hypothesized
that the dispersed S. mutans might utilize DeoC to degrade NETs and escape
killing by the immune system. It was found that S. mutans induced NET formation
upon contact with neutrophils, while the presence of NETs in turn enhanced the
deoC expression of S. mutans. Fluorescence microscopy inspection showed that deoC
deletion resulted in a decreased NET degradation ability of S. mutans and
enhanced susceptibility to neutrophil killing. Data obtained from this study
assigned two important roles for DeoC in S. mutans: contributing to the spread of
infection through mediating biofilm dispersal, and facilitating the escape of S.
mutans from neutrophil killing through NET degradation.