Spd1672 gene knockout significantly attenuates the virulence of Streptococcus pneumoniae.
- Author:
Jian HUANG
1
;
MeiRong HUANG
;
Kaifeng WU
;
Jiehua ZHU
;
Bing LI
;
Xun MIN
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Bacterial Proteins; genetics; Cell Line, Tumor; Gene Knockout Techniques; Humans; Mice; Mice, Inbred BALB C; Streptococcus pneumoniae; genetics; pathogenicity; Virulence
- From: Journal of Southern Medical University 2015;35(8):1197-1200
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the role of spd1672 gene in the infection process of Streptococcus pneumoniae.
METHODSBALB/c mice were intraperitoneally infected by a spd1672 knockout strain and a D39 wild-type strain of S. pneumoniae, and the survival time of mice and blood bacterial counts were recorded. The adhesion and invasion ability of S. pneumoniae strains were assessed in A549 cells. Bactericidal assays were carried out to determine the resistance of spd1672 knockout strains and D39 wild strains, and the serum levels of inflammatory cytokines were detected in the infected mice.
RESULTSThe mice infected with spd1672 knockout strains showed a significantly longer median survival time, a higher survival rate, and a lower blood bacterial load than the wild strain-infected mice (P<0.05). Having a similar cell adhesion ability to the wild-type strain (P>0.05), the spd1672 knockout strain showed significantly lower cell invasion ability than the wild-type strain (P<0.05). The spd1672 knockout strain also had a reduced resistance to whole blood cells, and thw mice infected with spd1672 knockout strain exhibit lower levels of serum inflammatory cytokines than those infected with the wild-type strain.
CONCLUSIONSpd1672 gene is importantly related to the virulence of S. pneumoniae and plays important roles in modulating bacterial invasion, resistance to whole blood cells and proinflammatory responses.