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10.1016/j.chom.2016.06.003 http://scihub22266oqcxt.onion/10.1016/j.chom.2016.06.003 C5382021!5382021 !27414497     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27414497 &cmd=llinks): Failed to open stream: HTTP request failed! 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Group B Streptococcus Degrades Cyclic-di-AMP to Modulate STING-Dependent Type I Interferon Production |pdf=|usr=}}{{27414497 }} gab.com Text Group B Streptococcus Degrades Cyclic-di-AMP to Modulate STING-Dependent Type I Interferon Production JO: Cell Host Microbe http://www.kidney.de/pget.php?&tw=1&pmid=27414497 #FOAvip Induction of type I interferon (IFN) in response to microbial pathogens depends on a conserved cGAS-STING signaling pathway. The presence of DNA in the cytoplasm activates cGAS, while STING is activated by cyclic dinucleotides (cdNs) produced by cGAS or from bacterial origins. Here, we show that Group B Streptococcus (GBS) induces IFN-? production almost exclusively through cGAS-STING-dependent recognition of bacterial DNA. However, we find that GBS expresses an ectonucleotidase, CdnP, which hydrolyzes extracellular bacterial cyclic-di-AMP. Inactivation of CdnP leads to c-di-AMP accumulation outside the bacteria and increased IFN-? production. Higher IFN-? levels in vivo increase GBS killing by the host. The IFN-? overproduction observed in the absence of CdnP is due to the cumulative effect of DNA sensing by cGAS and STING-dependent sensing of c-di-AMP. These findings describe the importance of a bacterial c-di-AMP ectonucleotidase and suggest a direct bacterial mechanism that dampens activation of the cGAS-STING axis. Twit Text FOAVip Group B Streptococcus Degrades Cyclic-di-AMP to Modulate STING-Dependent Type I Interferon Production ????Cell Host Microbe http://www.kidney.de/pget.php?&tw=1&pmid=27414497 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27414497 #FOAvip English Wikipedia <ref>{{Cite pmid|27414497 }}</ref> Group B Streptococcus Degrades Cyclic-di-AMP to Modulate STING-Dependent Type I Interferon Production #MMPMID27414497 Andrade WA ; Firon A ; Schmidt T ; Hornung V ; Fitzgerald KA ; Kurt-Jones EA ; Trieu-Cuot P ; Golenbock DT ; Kaminski PA Cell Host Microbe 2016[Jul]; 20 (1 ): 49-59 PMID27414497 show ga Induction of type I interferon (IFN) in response to microbial pathogens depends on a conserved cGAS-STING signaling pathway. The presence of DNA in the cytoplasm activates cGAS, while STING is activated by cyclic dinucleotides (cdNs) produced by cGAS or from bacterial origins. Here, we show that Group B Streptococcus (GBS) induces IFN-? production almost exclusively through cGAS-STING-dependent recognition of bacterial DNA. However, we find that GBS expresses an ectonucleotidase, CdnP, which hydrolyzes extracellular bacterial cyclic-di-AMP. Inactivation of CdnP leads to c-di-AMP accumulation outside the bacteria and increased IFN-? production. Higher IFN-? levels in vivo increase GBS killing by the host. The IFN-? overproduction observed in the absence of CdnP is due to the cumulative effect of DNA sensing by cGAS and STING-dependent sensing of c-di-AMP. These findings describe the importance of a bacterial c-di-AMP ectonucleotidase and suggest a direct bacterial mechanism that dampens activation of the cGAS-STING axis. |*Immune Evasion [MESH] |Biotransformation [MESH] |Dinucleoside Phosphates/*metabolism [MESH] |Interferon Type I/*metabolism [MESH] |Membrane Proteins/*metabolism [MESH] |Pyrophosphatases/*metabolism [MESH]Group B Streptococcus Degrades Cyclic-di-AMP to Modulate STING-Depende(epmc).pdf DeepDyve Pubget Overpricing