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10.1111/cmi.12560 http://scihub22266oqcxt.onion/10.1111/cmi.12560 C5101013!5101013 !26687842     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26687842 &cmd=llinks): Failed to open stream: HTTP request failed! 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Fusobacterium nucleatum infection of gingival epithelial cells leads to NLRP3 inflammasome-dependent secretion of IL-1? and the danger signals ASC and HMGB1 |pdf=|usr=}}{{26687842 }} gab.com Text Fusobacterium nucleatum infection of gingival epithelial cells leads to NLRP3 inflammasome-dependent secretion of IL-1 and the danger signals ASC and HMGB1 JO: Cell Microbiol http://www.kidney.de/pget.php?&tw=1&pmid=26687842 #FOAvip Fusobacterium nucleatum is an invasive anaerobic bacterium that is associated with periodontal disease. Previous studies have focused on virulence factors produced by F. nucleatum, but early recognition of the pathogen by the immune system remains poorly understood. Although an inflammasome in gingival epithelial cells (GECs) can be stimulated by danger-associated molecular patterns (DAMPs) (also known as danger signals) such as ATP, inflammasome activation by this periodontal pathogen has yet to be described in these cells. This study therefore examines the effects of F. nucleatum infection on pro-inflammatory cytokine expression and inflammasome activation in GECs. Our results indicate that infection induces translocation of NF-?B into the nucleus, resulting in cytokine gene expression. In addition, infection activates the NLRP3 inflammasome, which in turn activates caspase-1 and stimulates secretion of mature IL-1?. Unlike other pathogens studied until now, F. nucleatum activates the inflammasome in GECs in the absence of exogenous DAMPs such as ATP. Finally, infection promotes release of other DAMPs that mediate inflammation, such as high-mobility group box 1 protein and apoptosis-associated speck-like protein, with a similar time-course as caspase-1 activation. Thus, F. nucleatum expresses the pathogen-associated molecular patterns necessary to activate NF-?B and also provides an endogenous DAMP to stimulate the inflammasome and further amplify inflammation through secretion of secondary DAMPs. Twit Text FOAVip Fusobacterium nucleatum infection of gingival epithelial cells leads to NLRP3 inflammasome-dependent secretion of IL-1 and the danger signals ASC and HMGB1 ????Cell Microbiol http://www.kidney.de/pget.php?&tw=1&pmid=26687842 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26687842 #FOAvip English Wikipedia <ref>{{Cite pmid|26687842 }}</ref> Fusobacterium nucleatum infection of gingival epithelial cells leads to NLRP3 inflammasome-dependent secretion of IL-1? and the danger signals ASC and HMGB1 #MMPMID26687842 Bui FQ ; Johnson L ; Roberts J ; Hung SC ; Lee J ; Atanasova KR ; Huang PR ; Yilmaz Ö ; Ojcius DM Cell Microbiol 2016[Jul]; 18 (7 ): 970-81 PMID26687842 show ga Fusobacterium nucleatum is an invasive anaerobic bacterium that is associated with periodontal disease. Previous studies have focused on virulence factors produced by F. nucleatum, but early recognition of the pathogen by the immune system remains poorly understood. Although an inflammasome in gingival epithelial cells (GECs) can be stimulated by danger-associated molecular patterns (DAMPs) (also known as danger signals) such as ATP, inflammasome activation by this periodontal pathogen has yet to be described in these cells. This study therefore examines the effects of F. nucleatum infection on pro-inflammatory cytokine expression and inflammasome activation in GECs. Our results indicate that infection induces translocation of NF-?B into the nucleus, resulting in cytokine gene expression. In addition, infection activates the NLRP3 inflammasome, which in turn activates caspase-1 and stimulates secretion of mature IL-1?. Unlike other pathogens studied until now, F. nucleatum activates the inflammasome in GECs in the absence of exogenous DAMPs such as ATP. Finally, infection promotes release of other DAMPs that mediate inflammation, such as high-mobility group box 1 protein and apoptosis-associated speck-like protein, with a similar time-course as caspase-1 activation. Thus, F. nucleatum expresses the pathogen-associated molecular patterns necessary to activate NF-?B and also provides an endogenous DAMP to stimulate the inflammasome and further amplify inflammation through secretion of secondary DAMPs. |CARD Signaling Adaptor Proteins [MESH] |Caspase 1/metabolism [MESH] |Cell Line [MESH] |Cytoskeletal Proteins/*metabolism [MESH] |Epithelial Cells/metabolism/microbiology [MESH] |Fusobacterium Infections/*metabolism/microbiology [MESH] |Fusobacterium nucleatum/pathogenicity [MESH] |Gingiva/cytology/metabolism/*microbiology [MESH] |HMGB1 Protein/*metabolism [MESH] |Host-Pathogen Interactions/physiology [MESH] |Humans [MESH] |Inflammasomes/metabolism [MESH] |Interleukin-1beta/genetics/*metabolism [MESH] |NF-kappa B/metabolism [MESH] |NLR Family, Pyrin Domain-Containing 3 Protein/genetics/metabolism [MESH]Fusobacterium nucleatum infection of gingival epithelial cells leads t(epmc).pdf DeepDyve Pubget Overpricing