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10.1073/pnas.1419925111 http://scihub22266oqcxt.onion/10.1073/pnas.1419925111 C4267384!4267384!25422455     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       Proc+Natl+Acad+Sci+U+S+A 2014 ; 111 (49): 17588-93 Nephropedia Template TP {{tp|p=25422455|t=2014. Actin polymerization as a key innate immune effector mechanism to control Salmonella infection |pdf=|usr=}}{{25422455}} gab.com Text Actin polymerization as a key innate immune effector mechanism to control Salmonella infection JO: Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=25422455 #FOAvip Infectious diseases are responsible for one-third of all mortality worldwide. Innate immunity is critical for mounting host defenses that eliminate pathogens. Salmonella is a global food-borne pathogen that infects and replicates within macrophages. How inflammasomes?multimeric protein complexes that provide innate immune protection?function to restrict bacterial burden in macrophages remains unknown. We show that actin polymerization is critical for NLRC4 inflammasome activation in response to Salmonella infection. NLRC4 activation in Salmonella-infected cells prevents further uptake of bacteria by inducing cellular stiffness and antimicrobial responses, which prevent bacterial dissemination in the host. These results demonstrate a critical link between innate immunity and the actin cytoskeleton in the cellular defense against Salmonella infection. Twit Text FOAVip Actin polymerization as a key innate immune effector mechanism to control Salmonella infection ????Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=25422455 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25422455 #FOAvip English Wikipedia <ref>{{Cite pmid|25422455}}</ref> Actin polymerization as a key innate immune effector mechanism to control Salmonella infection #MMPMID25422455 Man SM; Ekpenyong A; Tourlomousis P; Achouri S; Cammarota E; Hughes K; Rizzo A; Ng G; Wright JA; Cicuta P; Guck JR; Bryant CE Proc Natl Acad Sci U S A 2014[Dec]; 111 (49): 17588-93 PMID25422455show ga Infectious diseases are responsible for one-third of all mortality worldwide. Innate immunity is critical for mounting host defenses that eliminate pathogens. Salmonella is a global food-borne pathogen that infects and replicates within macrophages. How inflammasomes?multimeric protein complexes that provide innate immune protection?function to restrict bacterial burden in macrophages remains unknown. We show that actin polymerization is critical for NLRC4 inflammasome activation in response to Salmonella infection. NLRC4 activation in Salmonella-infected cells prevents further uptake of bacteria by inducing cellular stiffness and antimicrobial responses, which prevent bacterial dissemination in the host. These results demonstrate a critical link between innate immunity and the actin cytoskeleton in the cellular defense against Salmonella infection. äActin polymerization as a key innate immune effector mechanism to cont(epmc).pdf DeepDyve Pubget Overpricing