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10.1371/journal.ppat.1006383 http://scihub22266oqcxt.onion/10.1371/journal.ppat.1006383 C5453623!5453623 !28570638     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28570638 &cmd=llinks): Failed to open stream: HTTP request failed! 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Detection of a microbial metabolite by STING regulates inflammasome activation in response to Chlamydia trachomatis infection |pdf=|usr=}}{{28570638 }} gab.com Text Detection of a microbial metabolite by STING regulates inflammasome activation in response to Chlamydia trachomatis infection JO: PLoS Pathog http://www.kidney.de/pget.php?&tw=1&pmid=28570638 #FOAvip The innate immune system is a critical component of host defence against microbial pathogens, but effective responses require an ability to distinguish between infectious and non-infectious insult to prevent inappropriate inflammation. Using the important obligate intracellular human pathogen Chlamydia trachomatis; an organism that causes significant immunopathology, we sought to determine critical host and pathogen factors that contribute to the induction of inflammasome activation. We assayed inflammasome activation by immunoblotting and ELISA to detect IL-1? processing and LDH release to determine pyroptosis. Using primary murine bone marrow derived macrophages or human monocyte derived dendritic cells, infected with live or attenuated Chlamydia trachomatis we report that the live organism activates both canonical and non-canonical inflammasomes, but only canonical inflammasomes controlled IL-1? processing which preceded pyroptosis. NADPH oxidase deficient macrophages were permissive to Chlamydia trachomatis replication and displayed elevated type-1 interferon and inflammasome activation. Conversely, attenuated, non-replicating Chlamydia trachomatis, primed but did not activate inflammasomes and stimulated reduced type-1 interferon responses. This suggested bacterial replication or metabolism as important factors that determine interferon responses and inflammasome activation. We identified STING but not cGAS as a central mediator of interferon regulated inflammasome activation. Interestingly, exogenous delivery of a Chlamydia trachomatis metabolite and STING ligand-cyclic di-AMP, recovered inflammasome activation to attenuated bacteria in a STING dependent manner thus indicating that a bacterial metabolite is a key factor initiating inflammasome activation through STING, independent of cGAS. These data suggest a potential mechanism of how the innate immune system can distinguish between infectious and non-infectious insult and instigate appropriate immune responses that could be therapeutically targeted. Twit Text FOAVip Detection of a microbial metabolite by STING regulates inflammasome activation in response to Chlamydia trachomatis infection ????PLoS Pathog http://www.kidney.de/pget.php?&tw=1&pmid=28570638 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28570638 #FOAvip English Wikipedia <ref>{{Cite pmid|28570638 }}</ref> Detection of a microbial metabolite by STING regulates inflammasome activation in response to Chlamydia trachomatis infection #MMPMID28570638 Webster SJ ; Brode S ; Ellis L ; Fitzmaurice TJ ; Elder MJ ; Gekara NO ; Tourlomousis P ; Bryant C ; Clare S ; Chee R ; Gaston HJS ; Goodall JC PLoS Pathog 2017[Jun]; 13 (6 ): e1006383 PMID28570638 show ga The innate immune system is a critical component of host defence against microbial pathogens, but effective responses require an ability to distinguish between infectious and non-infectious insult to prevent inappropriate inflammation. Using the important obligate intracellular human pathogen Chlamydia trachomatis; an organism that causes significant immunopathology, we sought to determine critical host and pathogen factors that contribute to the induction of inflammasome activation. We assayed inflammasome activation by immunoblotting and ELISA to detect IL-1? processing and LDH release to determine pyroptosis. Using primary murine bone marrow derived macrophages or human monocyte derived dendritic cells, infected with live or attenuated Chlamydia trachomatis we report that the live organism activates both canonical and non-canonical inflammasomes, but only canonical inflammasomes controlled IL-1? processing which preceded pyroptosis. NADPH oxidase deficient macrophages were permissive to Chlamydia trachomatis replication and displayed elevated type-1 interferon and inflammasome activation. Conversely, attenuated, non-replicating Chlamydia trachomatis, primed but did not activate inflammasomes and stimulated reduced type-1 interferon responses. This suggested bacterial replication or metabolism as important factors that determine interferon responses and inflammasome activation. We identified STING but not cGAS as a central mediator of interferon regulated inflammasome activation. Interestingly, exogenous delivery of a Chlamydia trachomatis metabolite and STING ligand-cyclic di-AMP, recovered inflammasome activation to attenuated bacteria in a STING dependent manner thus indicating that a bacterial metabolite is a key factor initiating inflammasome activation through STING, independent of cGAS. These data suggest a potential mechanism of how the innate immune system can distinguish between infectious and non-infectious insult and instigate appropriate immune responses that could be therapeutically targeted. |Animals [MESH] |Chlamydia Infections/*immunology/*microbiology [MESH] |Chlamydia trachomatis/genetics/immunology/*physiology [MESH] |Cyclic AMP/immunology [MESH] |Dendritic Cells/immunology/microbiology [MESH] |Female [MESH] |Humans [MESH] |Inflammasomes/*immunology [MESH] |Interferon Type I/genetics/immunology [MESH] |Interleukin-1beta/genetics/immunology [MESH] |Macrophages/*immunology/microbiology [MESH] |Male [MESH] |Membrane Proteins/genetics/*immunology [MESH] |Mice [MESH]Detection of a microbial metabolite by STING regulates inflammasome ac(epmc).pdf DeepDyve Pubget Overpricing