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10.1371/journal.ppat.1005804 http://scihub22266oqcxt.onion/10.1371/journal.ppat.1005804 C4978498!4978498!27505057     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 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       PLoS+Pathog 2016 ; 12 (8): ä Nephropedia Template TP {{tp|p=27505057|t=2016. An Epithelial Integrin Regulates the Amplitude of Protective Lung Interferon Responses against Multiple Respiratory Pathogens |pdf=|usr=}}{{27505057}} gab.com Text An Epithelial Integrin Regulates the Amplitude of Protective Lung Interferon Responses against Multiple Respiratory Pathogens JO: PLoS Pathog http://www.kidney.de/pget.php?&tw=1&pmid=27505057 #FOAvip The healthy lung maintains a steady state of immune readiness to rapidly respond to injury from invaders. Integrins are important for setting the parameters of this resting state, particularly the epithelial-restricted ?V?6 integrin, which is upregulated during injury. Once expressed, ?V?6 moderates acute lung injury (ALI) through as yet undefined molecular mechanisms. We show that the upregulation of ?6 during influenza infection is involved in disease pathogenesis. ?6-deficient mice (?6 KO) have increased survival during influenza infection likely due to the limited viral spread into the alveolar spaces leading to reduced ALI. Although the ?6 KO have morphologically normal lungs, they harbor constitutively activated lung CD11b+ alveolar macrophages (AM) and elevated type I IFN signaling activity, which we traced to the loss of ?6-activated transforming growth factor-? (TGF-?). Administration of exogenous TGF-? to ?6 KO mice leads to reduced numbers of CD11b+ AMs, decreased type I IFN signaling activity and loss of the protective phenotype during influenza infection. Protection extended to other respiratory pathogens such as Sendai virus and bacterial pneumonia. Our studies demonstrate that the loss of one epithelial protein, ?V?6 integrin, can alter the lung microenvironment during both homeostasis and respiratory infection leading to reduced lung injury and improved survival. Twit Text FOAVip An Epithelial Integrin Regulates the Amplitude of Protective Lung Interferon Responses against Multiple Respiratory Pathogens ????PLoS Pathog http://www.kidney.de/pget.php?&tw=1&pmid=27505057 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27505057 #FOAvip English Wikipedia <ref>{{Cite pmid|27505057}}</ref> An Epithelial Integrin Regulates the Amplitude of Protective Lung Interferon Responses against Multiple Respiratory Pathogens #MMPMID27505057 Meliopoulos VA; Van de Velde LA; Van de Velde NC; Karlsson EA; Neale G; Vogel P; Guy C; Sharma S; Duan S; Surman SL; Jones BG; Johnson MDL; Bosio C; Jolly L; Jenkins RG; Hurwitz JL; Rosch JW; Sheppard D; Thomas PG; Murray PJ; Schultz-Cherry S PLoS Pathog 2016[Aug]; 12 (8): ä PMID27505057show ga The healthy lung maintains a steady state of immune readiness to rapidly respond to injury from invaders. Integrins are important for setting the parameters of this resting state, particularly the epithelial-restricted ?V?6 integrin, which is upregulated during injury. Once expressed, ?V?6 moderates acute lung injury (ALI) through as yet undefined molecular mechanisms. We show that the upregulation of ?6 during influenza infection is involved in disease pathogenesis. ?6-deficient mice (?6 KO) have increased survival during influenza infection likely due to the limited viral spread into the alveolar spaces leading to reduced ALI. Although the ?6 KO have morphologically normal lungs, they harbor constitutively activated lung CD11b+ alveolar macrophages (AM) and elevated type I IFN signaling activity, which we traced to the loss of ?6-activated transforming growth factor-? (TGF-?). Administration of exogenous TGF-? to ?6 KO mice leads to reduced numbers of CD11b+ AMs, decreased type I IFN signaling activity and loss of the protective phenotype during influenza infection. Protection extended to other respiratory pathogens such as Sendai virus and bacterial pneumonia. Our studies demonstrate that the loss of one epithelial protein, ?V?6 integrin, can alter the lung microenvironment during both homeostasis and respiratory infection leading to reduced lung injury and improved survival. äAn Epithelial Integrin Regulates the Amplitude of Protective Lung Inte(epmc).pdf DeepDyve Pubget Overpricing