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10.4049/jimmunol.1300014 http://scihub22266oqcxt.onion/10.4049/jimmunol.1300014 C4907362!4907362!23804714     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Immunol 2013 ; 191 (3): 1250-9 Nephropedia Template TP {{tp|p=23804714|t=2013. Depletion of alveolar macrophages during influenza infection facilitates bacterial super-infections |pdf=|usr=}}{{23804714}} gab.com Text Depletion of alveolar macrophages during influenza infection facilitates bacterial super-infections JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=23804714 #FOAvip Viruses such as influenza suppress host immune function by a variety of methods. This may result in significant morbidity through several pathways, including facilitation of secondary bacterial pneumonia from pathogens such as Streptococcus pneumoniae. PKH26-PCL dye was administered intranasally to label resident alveolar macrophages (AMs) in a well-established murine model prior to influenza infection to determine turnover kinetics during the course of infection. More than 90% of resident AMs were lost in the first week after influenza, while the remaining cells had a necrotic phenotype. To establish the impact of this innate immune defect, influenza-infected mice were challenged with S. pneumoniae. Early AM-mediated bacterial clearance was significantly impaired in influenza-infected mice - about 50% of the initial bacterial inoculum could be harvested from the alveolar airspace 3 hours later. In mock-infected mice, by contrast, more than 95% of inocula up-to-50-fold higher was efficiently cleared. Co-infection during the AM depletion phase caused significant body weight loss and mortality. Two weeks after influenza, the AM population was fully replenished with successful re-establishment of early innate host protection. Local GM-CSF treatment partially restored the impaired early bacterial clearance with efficient protection against secondary pneumococcal pneumonia. We conclude that resident AM depletion occurs during influenza infection. Among other potential effects, this establishes a niche for secondary pneumococcal infection by altering early cellular innate immunity in the lungs resulting in pneumococcal outgrowth and lethal pneumonia. This novel mechanism will inform development of novel therapeutic approaches to restore lung innate immunity against bacterial super-infections. Twit Text FOAVip Depletion of alveolar macrophages during influenza infection facilitates bacterial super-infections ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=23804714 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23804714 #FOAvip English Wikipedia <ref>{{Cite pmid|23804714}}</ref> Depletion of alveolar macrophages during influenza infection facilitates bacterial super-infections #MMPMID23804714 Ghoneim HE; Thomas PG; McCullers JA J Immunol 2013[Aug]; 191 (3): 1250-9 PMID23804714show ga Viruses such as influenza suppress host immune function by a variety of methods. This may result in significant morbidity through several pathways, including facilitation of secondary bacterial pneumonia from pathogens such as Streptococcus pneumoniae. PKH26-PCL dye was administered intranasally to label resident alveolar macrophages (AMs) in a well-established murine model prior to influenza infection to determine turnover kinetics during the course of infection. More than 90% of resident AMs were lost in the first week after influenza, while the remaining cells had a necrotic phenotype. To establish the impact of this innate immune defect, influenza-infected mice were challenged with S. pneumoniae. Early AM-mediated bacterial clearance was significantly impaired in influenza-infected mice - about 50% of the initial bacterial inoculum could be harvested from the alveolar airspace 3 hours later. In mock-infected mice, by contrast, more than 95% of inocula up-to-50-fold higher was efficiently cleared. Co-infection during the AM depletion phase caused significant body weight loss and mortality. Two weeks after influenza, the AM population was fully replenished with successful re-establishment of early innate host protection. Local GM-CSF treatment partially restored the impaired early bacterial clearance with efficient protection against secondary pneumococcal pneumonia. We conclude that resident AM depletion occurs during influenza infection. Among other potential effects, this establishes a niche for secondary pneumococcal infection by altering early cellular innate immunity in the lungs resulting in pneumococcal outgrowth and lethal pneumonia. This novel mechanism will inform development of novel therapeutic approaches to restore lung innate immunity against bacterial super-infections. äDepletion of alveolar macrophages during influenza infection facilitat(epmc).pdf DeepDyve Pubget Overpricing