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10.1371/journal.ppat.1002736 http://scihub22266oqcxt.onion/10.1371/journal.ppat.1002736 22719247!3375267!22719247     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=22719247&cmd=llinks): Failed to open stream: HTTP request failed! 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DNase Sda1 allows invasive M1T1 Group A Streptococcus to prevent TLR9-dependent recognition |pdf=|usr=}}{{22719247}} gab.com Text DNase Sda1 allows invasive M1T1 Group A Streptococcus to prevent TLR9-dependent recognition JO: PLoS Pathog http://www.kidney.de/pget.php?&tw=1&pmid=22719247 #FOAvip Group A Streptococcus (GAS) has developed a broad arsenal of virulence factors that serve to circumvent host defense mechanisms. The virulence factor DNase Sda1 of the hyperinvasive M1T1 GAS clone degrades DNA-based neutrophil extracellular traps allowing GAS to escape extracellular killing. TLR9 is activated by unmethylated CpG-rich bacterial DNA and enhances innate immune resistance. We hypothesized that Sda1 degradation of bacterial DNA could alter TLR9-mediated recognition of GAS by host innate immune cells. We tested this hypothesis using a dual approach: loss and gain of function of DNase in isogenic GAS strains and presence and absence of TLR9 in the host. Either DNA degradation by Sda1 or host deficiency of TLR9 prevented GAS induced IFN-alpha and TNF-alpha secretion from murine macrophages and contributed to bacterial survival. Similarly, in a murine necrotizing fasciitis model, IFN-alpha and TNF-alpha levels were significantly decreased in wild type mice infected with GAS expressing Sda1, whereas no such Sda1-dependent effect was seen in a TLR9-deficient background. Thus GAS Sda1 suppressed both the TLR9-mediated innate immune response and macrophage bactericidal activity. Our results demonstrate a novel mechanism of bacterial innate immune evasion based on autodegradation of CpG-rich DNA by a bacterial DNase. Twit Text FOAVip DNase Sda1 allows invasive M1T1 Group A Streptococcus to prevent TLR9-dependent recognition ????PLoS Pathog http://www.kidney.de/pget.php?&tw=1&pmid=22719247 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=22719247 #FOAvip English Wikipedia <ref>{{Cite pmid|22719247}}</ref> DNase Sda1 allows invasive M1T1 Group A Streptococcus to prevent TLR9-dependent recognition #MMPMID22719247 Uchiyama S; Andreoni F; Schuepbach RA; Nizet V; Zinkernagel AS PLoS Pathog 2012[]; 8 (6): e1002736 PMID22719247show ga Group A Streptococcus (GAS) has developed a broad arsenal of virulence factors that serve to circumvent host defense mechanisms. The virulence factor DNase Sda1 of the hyperinvasive M1T1 GAS clone degrades DNA-based neutrophil extracellular traps allowing GAS to escape extracellular killing. TLR9 is activated by unmethylated CpG-rich bacterial DNA and enhances innate immune resistance. We hypothesized that Sda1 degradation of bacterial DNA could alter TLR9-mediated recognition of GAS by host innate immune cells. We tested this hypothesis using a dual approach: loss and gain of function of DNase in isogenic GAS strains and presence and absence of TLR9 in the host. Either DNA degradation by Sda1 or host deficiency of TLR9 prevented GAS induced IFN-alpha and TNF-alpha secretion from murine macrophages and contributed to bacterial survival. Similarly, in a murine necrotizing fasciitis model, IFN-alpha and TNF-alpha levels were significantly decreased in wild type mice infected with GAS expressing Sda1, whereas no such Sda1-dependent effect was seen in a TLR9-deficient background. Thus GAS Sda1 suppressed both the TLR9-mediated innate immune response and macrophage bactericidal activity. Our results demonstrate a novel mechanism of bacterial innate immune evasion based on autodegradation of CpG-rich DNA by a bacterial DNase. |Animals[MESH] |Cytokines/biosynthesis/immunology[MESH] |DNA, Bacterial/metabolism[MESH] |Deoxyribonuclease I/immunology/*metabolism[MESH] |Enzyme-Linked Immunosorbent Assay[MESH] |Host-Parasite Interactions/*physiology[MESH] |Humans[MESH] |Immune Evasion/*physiology[MESH] |Macrophages/immunology/virology[MESH] |Mice[MESH] |Mice, Inbred C57BL[MESH] |Mice, Knockout[MESH] |Streptococcal Infections/immunology/*metabolism[MESH] |Streptococcus pyogenes/immunology/metabolism/*pathogenicity[MESH] |Toll-Like Receptor 9/immunology/*metabolism[MESH]DNase Sda1 allows invasive M1T1 Group A Streptococcus to prevent TLR9-(epmc).pdf DeepDyve Pubget Overpricing