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10.1128/IAI.00297-17 http://scihub22266oqcxt.onion/10.1128/IAI.00297-17 28947649!5695129!28947649     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28947649&cmd=llinks): Failed to open stream: HTTP request failed! 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Modulation of Neutrophil Extracellular Trap and Reactive Oxygen Species Release by Periodontal Bacteria |pdf=|usr=}}{{28947649}} gab.com Text Modulation of Neutrophil Extracellular Trap and Reactive Oxygen Species Release by Periodontal Bacteria JO: Infect Immun http://www.kidney.de/pget.php?&tw=1&pmid=28947649 #FOAvip Oral bacteria are the main trigger for the development of periodontitis, and some species are known to modulate neutrophil function. This study aimed to explore the release of neutrophil extracellular traps (NETs), associated antimicrobial proteins, and reactive oxygen species (ROS) in response to periodontal bacteria, as well as the underlying pathways. Isolated peripheral blood neutrophils were stimulated with 19 periodontal bacteria. NET and ROS release, as well as the expression of NET-bound antimicrobial proteins, elastase, myeloperoxidase, and cathepsin G, in response to these species was measured using fluorescence-based assays. NET and ROS release was monitored after the addition of NADP (NADPH) oxidase pathway modulators and inhibitors of Toll-like receptors (TLRs). Moreover, bacterial entrapment by NETs was visualized microscopically, and bacterial killing was assessed by bacterial culture. Certain microorganisms, e.g., Veillonella parvula and Streptococcus gordonii, stimulated higher levels of ROS and NET release than others. NETs were found to entrap, but not kill, all periodontal bacteria tested. NADPH oxidase pathway modulators decreased ROS production but not NET production in response to the bacteria. Interestingly, TLR inhibitors did not impact ROS and NET release. These data suggest that the variability in the neutrophil response toward different bacteria may contribute to the pathogenesis of periodontal diseases by mechanisms such as bacterial avoidance of host responses and activation of neutrophils. Moreover, our results indicate that bacterium-stimulated NET release may arise in part via NADPH oxidase-independent mechanisms. The role of TLR signaling in bacterium-induced ROS and NET release needs to be further elucidated. Twit Text FOAVip Modulation of Neutrophil Extracellular Trap and Reactive Oxygen Species Release by Periodontal Bacteria ????Infect Immun http://www.kidney.de/pget.php?&tw=1&pmid=28947649 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28947649 #FOAvip English Wikipedia <ref>{{Cite pmid|28947649}}</ref> Modulation of Neutrophil Extracellular Trap and Reactive Oxygen Species Release by Periodontal Bacteria #MMPMID28947649 Hirschfeld J; White PC; Milward MR; Cooper PR; Chapple ILC Infect Immun 2017[Dec]; 85 (12): ä PMID28947649show ga Oral bacteria are the main trigger for the development of periodontitis, and some species are known to modulate neutrophil function. This study aimed to explore the release of neutrophil extracellular traps (NETs), associated antimicrobial proteins, and reactive oxygen species (ROS) in response to periodontal bacteria, as well as the underlying pathways. Isolated peripheral blood neutrophils were stimulated with 19 periodontal bacteria. NET and ROS release, as well as the expression of NET-bound antimicrobial proteins, elastase, myeloperoxidase, and cathepsin G, in response to these species was measured using fluorescence-based assays. NET and ROS release was monitored after the addition of NADP (NADPH) oxidase pathway modulators and inhibitors of Toll-like receptors (TLRs). Moreover, bacterial entrapment by NETs was visualized microscopically, and bacterial killing was assessed by bacterial culture. Certain microorganisms, e.g., Veillonella parvula and Streptococcus gordonii, stimulated higher levels of ROS and NET release than others. NETs were found to entrap, but not kill, all periodontal bacteria tested. NADPH oxidase pathway modulators decreased ROS production but not NET production in response to the bacteria. Interestingly, TLR inhibitors did not impact ROS and NET release. These data suggest that the variability in the neutrophil response toward different bacteria may contribute to the pathogenesis of periodontal diseases by mechanisms such as bacterial avoidance of host responses and activation of neutrophils. Moreover, our results indicate that bacterium-stimulated NET release may arise in part via NADPH oxidase-independent mechanisms. The role of TLR signaling in bacterium-induced ROS and NET release needs to be further elucidated. |*Extracellular Traps[MESH] |*Reactive Oxygen Species[MESH] |Antimicrobial Cationic Peptides/metabolism[MESH] |Bacteria, Anaerobic/*immunology[MESH] |Colony Count, Microbial[MESH] |Microbial Viability/drug effects[MESH] |Microscopy[MESH] |Neutrophils/*immunology[MESH] |Streptococcus gordonii/*immunology[MESH]Modulation of Neutrophil Extracellular Trap and Reactive Oxygen Specie(epmc).pdf DeepDyve Pubget Overpricing