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10.1093/infdis/jit830 http://scihub22266oqcxt.onion/10.1093/infdis/jit830 24367039!ä!24367039 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       J+Infect+Dis 2014 ; 209 (11): 1827-36 Nephropedia Template TP {{tp|p=24367039|t=2014. Protecting against post-influenza bacterial pneumonia by increasing phagocyte recruitment and ROS production |pdf=|usr=}}{{24367039}} gab.com Text Protecting against post-influenza bacterial pneumonia by increasing phagocyte recruitment and ROS production JO: J Infect Dis http://www.kidney.de/pget.php?&tw=1&pmid=24367039 #FOAvip Seasonal and especially pandemic influenza predispose patients to secondary bacterial pneumonias, which are a major cause of deaths and morbidity. Staphylococcus aureus is a particularly common and deadly form of post-influenza pneumonia, and increasing staphylococcal drug resistance makes the development of new therapies urgent. We explored an innate immune-mediated model of the lung to define novel mechanisms by which the host can be protected against secondary staphylococcal pneumonia after sub-lethal influenza infection. We found that stimulating the innate immunity in the lung by overexpression of GM-CSF will result in resistance to S. aureus pneumonia after sublethal influenza infection. Resistance was mediated by alveolar macrophages and neutrophils, and was associated with increased production of reactive oxygen species (ROS) by alveolar macrophages. Resistance was abrogated by treatment with agents that scavenged ROS. We conclude that stimulating innate immunity in the lung markedly reduces susceptibility to post-influenza staphylococcal pneumonia and that this may represent a novel immunomodulatory strategy for prevention and treatment of secondary bacterial pneumonia after influenza. Twit Text FOAVip Protecting against post-influenza bacterial pneumonia by increasing phagocyte recruitment and ROS production ????J Infect Dis http://www.kidney.de/pget.php?&tw=1&pmid=24367039 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24367039 #FOAvip English Wikipedia <ref>{{Cite pmid|24367039}}</ref> Protecting against post-influenza bacterial pneumonia by increasing phagocyte recruitment and ROS production #MMPMID24367039 Subramaniam R; Barnes PF; Fletcher K; Boggaram V; Hillberry Z; Neuenschwander P; Shams H J Infect Dis 2014[Jun]; 209 (11): 1827-36 PMID24367039show ga Seasonal and especially pandemic influenza predispose patients to secondary bacterial pneumonias, which are a major cause of deaths and morbidity. Staphylococcus aureus is a particularly common and deadly form of post-influenza pneumonia, and increasing staphylococcal drug resistance makes the development of new therapies urgent. We explored an innate immune-mediated model of the lung to define novel mechanisms by which the host can be protected against secondary staphylococcal pneumonia after sub-lethal influenza infection. We found that stimulating the innate immunity in the lung by overexpression of GM-CSF will result in resistance to S. aureus pneumonia after sublethal influenza infection. Resistance was mediated by alveolar macrophages and neutrophils, and was associated with increased production of reactive oxygen species (ROS) by alveolar macrophages. Resistance was abrogated by treatment with agents that scavenged ROS. We conclude that stimulating innate immunity in the lung markedly reduces susceptibility to post-influenza staphylococcal pneumonia and that this may represent a novel immunomodulatory strategy for prevention and treatment of secondary bacterial pneumonia after influenza. |Amphiregulin[MESH] |Animals[MESH] |Gene Expression Regulation/immunology[MESH] |Glycoproteins/genetics/metabolism[MESH] |Granulocyte-Macrophage Colony-Stimulating Factor/genetics/metabolism[MESH] |Influenza A Virus, H1N1 Subtype[MESH] |Intercellular Signaling Peptides and Proteins/genetics/metabolism[MESH] |Macrophages, Alveolar[MESH] |Neutrophils[MESH] |Orthomyxoviridae Infections/*complications/microbiology/virology[MESH] |Phagocytes/*physiology[MESH] |Pneumonia, Staphylococcal/*complications/microbiology[MESH] |Reactive Oxygen Species/*metabolism[MESH]Protecting against post-influenza bacterial pneumonia by increasing ph(epmc).pdf DeepDyve Pubget Overpricing