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10.1513/AnnalsATS.201402-056AW http://scihub22266oqcxt.onion/10.1513/AnnalsATS.201402-056AW C4298973!4298973!25525734     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 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       Ann+Am+Thorac+Soc 2014 ; 11 (Suppl 5): S287-91 Nephropedia Template TP {{tp|p=25525734|t=2014. Linking Acute Infection to Chronic Lung Disease The Role of IL-33?Expressing Epithelial Progenitor Cells |pdf=|usr=}}{{25525734}} gab.com Text Linking Acute Infection to Chronic Lung Disease The Role of IL-33 Expressing Epithelial Progenitor Cells JO: Ann Am Thorac Soc http://www.kidney.de/pget.php?&tw=1&pmid=25525734 #FOAvip Respiratory infection is a common feature of the major human airway diseases, such as asthma and chronic obstructive pulmonary disease, but the precise link between acute infection and chronic lung disease is still undefined. In a mouse model of this process, parainfluenza virus infection is followed by long-term induction of IL-33 expression and release and in turn innate immune cell generation of IL-13 and consequent airway disease signified by excess mucus formation. IL-33 induction was traceable to a subset of secretoglobin-positive airway epithelial cells linked to progenitor/stem cell function. In corresponding studies of humans with chronic obstructive pulmonary disease, an increase in IL-33 production was also detected in concert with up-regulation of IL-13 and airway mucus formation. In this case, increased IL-33 production was localized to a subset of airway basal cells that maintain an endogenous capacity for increased pluripotency and ATP-regulated release of IL-33 even ex vivo. The results provide evidence of a sustainable epithelial cell population that may be activated by environmental danger signals to release IL-33 and thereby lead to IL-13?dependent disease. The progenitor nature of this IL-33?expressing ATP-responsive cell population could explain an acquired susceptibility to chronic airway disease. The findings may therefore provide a new paradigm to explain the role of viral infection and the innate immune system in chronic lung disease based on the influence of long-term epithelial progenitor cells programmed for excess IL-33 production. Further studies are needed to address the basis for this type of postviral reprogramming and the means to correct it and thereby restore airway mucosal immune function to normal. Twit Text FOAVip Linking Acute Infection to Chronic Lung Disease The Role of IL-33 Expressing Epithelial Progenitor Cells ????Ann Am Thorac Soc http://www.kidney.de/pget.php?&tw=1&pmid=25525734 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25525734 #FOAvip English Wikipedia <ref>{{Cite pmid|25525734}}</ref> Linking Acute Infection to Chronic Lung Disease The Role of IL-33?Expressing Epithelial Progenitor Cells #MMPMID25525734 Holtzman MJ; Byers DE; Brett JA; Patel AC; Agapov E; Jin X; Wu K Ann Am Thorac Soc 2014[Dec]; 11 (Suppl 5): S287-91 PMID25525734show ga Respiratory infection is a common feature of the major human airway diseases, such as asthma and chronic obstructive pulmonary disease, but the precise link between acute infection and chronic lung disease is still undefined. In a mouse model of this process, parainfluenza virus infection is followed by long-term induction of IL-33 expression and release and in turn innate immune cell generation of IL-13 and consequent airway disease signified by excess mucus formation. IL-33 induction was traceable to a subset of secretoglobin-positive airway epithelial cells linked to progenitor/stem cell function. In corresponding studies of humans with chronic obstructive pulmonary disease, an increase in IL-33 production was also detected in concert with up-regulation of IL-13 and airway mucus formation. In this case, increased IL-33 production was localized to a subset of airway basal cells that maintain an endogenous capacity for increased pluripotency and ATP-regulated release of IL-33 even ex vivo. The results provide evidence of a sustainable epithelial cell population that may be activated by environmental danger signals to release IL-33 and thereby lead to IL-13?dependent disease. The progenitor nature of this IL-33?expressing ATP-responsive cell population could explain an acquired susceptibility to chronic airway disease. The findings may therefore provide a new paradigm to explain the role of viral infection and the innate immune system in chronic lung disease based on the influence of long-term epithelial progenitor cells programmed for excess IL-33 production. Further studies are needed to address the basis for this type of postviral reprogramming and the means to correct it and thereby restore airway mucosal immune function to normal. äLinking Acute Infection to Chronic Lung Disease The Role of IL-33?Exp(epmc).pdf DeepDyve Pubget Overpricing