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GHIP in Streptococcus pneumoniae is involved in antibacterial resistance and elicits a strong innate immune response through TLR 2 and JNK /p38 MAPK
Author(s) -
Dong Jie,
Wang Jian,
He Yujuan,
Li Chenwei,
Zhou Aie,
Cui Jin,
Xu Wenchun,
Zhong Liang,
Yin Yibing,
Zhang Xuemei,
Wang Hong
Publication year - 2014
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/febs.12903
Subject(s) - innate immune system , streptococcus pneumoniae , virulence factor , microbiology and biotechnology , biology , immune system , tumor necrosis factor alpha , virulence , mapk/erk pathway , pneumolysin , protein kinase a , lipopolysaccharide , signal transduction , immunology , kinase , biochemistry , gene , antibiotics
Interaction between pneumococcal virulence factors and innate immune receptors triggers host responses via specific signaling pathways after infection. By generating a deficient mutant, we show here that, compared with the wild‐type parent strain, glycosyl hydrolase 25 relating to invasion protein ( GHIP ) mutant strain was impaired in rapid dissemination into vessels and caused less severe inflammation in mice lungs. Further study demonstrated that the lack of this protein in Streptococcus pneumoniae caused an increased susceptibility to whole blood or neutrophils, while this impairment could be recovered by supplementing recombinant GHIP (r GHIP ). Additionally, secreted GHIP could be detected in culture medium, and purified protein was able to induce the release of tumor necrosis factor α and interleukin 6 from peritoneal macrophages. Further investigations revealed that the induction of interleukin 6 by this virulence factor depended on the phosphorylation of c‐Jun N‐terminal kinase and p38 mitogen activated protein kinase and Toll‐like receptor 2. Taken together, GHIP , a novel pneumococcal virulence factor, appeared to play a critical role in bacterial survival and the induction of host innate immune response during pneumococcal infection.