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10.1136/thoraxjnl-2017-210010 http://scihub22266oqcxt.onion/10.1136/thoraxjnl-2017-210010 C5969338!5969338!29079611     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Thorax 2018 ; 73 (6): 546-56 Nephropedia Template TP {{tp|p=29079611|t=2018. Neutrophils drive alveolar macrophage IL-1? release during respiratory viral infection |pdf=|usr=}}{{29079611}} gab.com Text Neutrophils drive alveolar macrophage IL-1 release during respiratory viral infection JO: Thorax http://www.kidney.de/pget.php?&tw=1&pmid=29079611 #FOAvip Background: Alveolar macrophages are sentinels of the airways that must exhibit immune restraint to innocuous antigens but elicit a robust inflammatory response to pathogenic threats. How distinction between these dichotomous functions is controlled is poorly defined.Neutrophils are the first responders to infection, and we hypothesised that they may free alveolar macrophages from their hyporesponsive state, promoting their activation. Activation of the inflammasome and interleukin (IL)-1? release is a key early inflammatory event that must be tightly regulated. Thus, the role of neutrophils in defining inflammasome activation in the alveolar macrophage was assessed. Methods: Mice were infected with the X31 strain of influenza virus and the role of neutrophils in alveolar macrophage activation established through administration of a neutrophil-depleting (1A8) antibody. Results: Influenza elicited a robust IL-1? release that correlated (r=0.6849; p<0.001) with neutrophil infiltrate and was ablated by neutrophil depletion. Alveolar macrophages were shown to be the prominent source of IL-1? during influenza infection, and virus triggered the expression of Nod-like receptor protein 3 (NLRP3) inflammasome and pro-IL-1? in these cells. However, subsequent activation of the inflammasome complex and release of mature IL-1? from alveolar macrophages were critically dependent on the provision of a secondary signal, in the form of antimicrobial peptide mCRAMP, from infiltrating neutrophils. Conclusions: Neutrophils are critical for the activation of the NLRP3 inflammasome in alveolar macrophages during respiratory viral infection. Accordingly, we rationalise that neutrophils are recruited to the lung to confront a viable pathogenic threat and subsequently commit alveolar macrophages to a pro-inflammatory phenotype to combat infection. Twit Text FOAVip Neutrophils drive alveolar macrophage IL-1 release during respiratory viral infection ????Thorax http://www.kidney.de/pget.php?&tw=1&pmid=29079611 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29079611 #FOAvip English Wikipedia <ref>{{Cite pmid|29079611}}</ref> Neutrophils drive alveolar macrophage IL-1? release during respiratory viral infection #MMPMID29079611 Peiró T; Patel DF; Akthar S; Gregory LG; Pyle CJ; Harker JA; Birrell MA; Lloyd CM; Snelgrove RJ Thorax 2018[Jun]; 73 (6): 546-56 PMID29079611show ga Background: Alveolar macrophages are sentinels of the airways that must exhibit immune restraint to innocuous antigens but elicit a robust inflammatory response to pathogenic threats. How distinction between these dichotomous functions is controlled is poorly defined.Neutrophils are the first responders to infection, and we hypothesised that they may free alveolar macrophages from their hyporesponsive state, promoting their activation. Activation of the inflammasome and interleukin (IL)-1? release is a key early inflammatory event that must be tightly regulated. Thus, the role of neutrophils in defining inflammasome activation in the alveolar macrophage was assessed. Methods: Mice were infected with the X31 strain of influenza virus and the role of neutrophils in alveolar macrophage activation established through administration of a neutrophil-depleting (1A8) antibody. Results: Influenza elicited a robust IL-1? release that correlated (r=0.6849; p<0.001) with neutrophil infiltrate and was ablated by neutrophil depletion. Alveolar macrophages were shown to be the prominent source of IL-1? during influenza infection, and virus triggered the expression of Nod-like receptor protein 3 (NLRP3) inflammasome and pro-IL-1? in these cells. However, subsequent activation of the inflammasome complex and release of mature IL-1? from alveolar macrophages were critically dependent on the provision of a secondary signal, in the form of antimicrobial peptide mCRAMP, from infiltrating neutrophils. Conclusions: Neutrophils are critical for the activation of the NLRP3 inflammasome in alveolar macrophages during respiratory viral infection. Accordingly, we rationalise that neutrophils are recruited to the lung to confront a viable pathogenic threat and subsequently commit alveolar macrophages to a pro-inflammatory phenotype to combat infection. äNeutrophils drive alveolar macrophage IL-1? release during respiratory(epmc).pdf DeepDyve Pubget Overpricing