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Streptococcus suis serotype 2 strains can induce the formation of neutrophil extracellular traps and evade trapping
Author(s) -
Jianqing Zhao,
Shan-Shan Pan,
Lan Lin,
Lei Fu,
Chao Yang,
Zhongmin Xu,
Yanmin Wei,
Meilin Jin,
Anding Zhang
Publication year - 2015
Publication title -
fems microbiology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 151
eISSN - 1574-6968
pISSN - 0378-1097
DOI - 10.1093/femsle/fnv022
Subject(s) - streptococcus suis , microbiology and biotechnology , phagocytosis , innate immune system , serotype , biology , neutrophil extracellular traps , strain (injury) , immune system , immunity , extracellular , virulence , immunology , gene , inflammation , genetics , anatomy
Streptococcus suis (S. suis) ranks among the five most important porcine pathogens worldwide and occasionally threatens human health, especially in people that come into close contact with pigs or pork products. Streptococcus suis serotype 2 (SS2) is considered to be the most pathogenic and prevalent capsular type. As a first line of immune defense against SS2 infection, neutrophils can eliminate the invader not only by phagocytosis but also by neutrophil extracellular traps (NETs)-mediated killing. SS2 can resist phagocytosis through polysaccharide capsule (CPS), but how this strain evades the effects of NETs remains to be determined. The present study demonstrated that the epidemic strain 05ZY, the highly pathogenic strain P1/7 and the intermediately pathogenic strain A7 could induce the formation of NETs. Furthermore, SS2 strains could successfully resist NETs-mediated killing, and the CPS structure contributed to this resistance by escaping the trapping. Therefore, the CPS structure not only contributed to the SS2 strains' resistance to phagocytosis-mediated killing but also played an essential role in evading NETs trapping and further killing in vitro. This study strengthens our understanding of how S. suis can evade innate immune surveillance and elimination.

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