Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.4049/jimmunol.1701406 http://scihub22266oqcxt.onion/10.4049/jimmunol.1701406 C6008236!6008236!29760191     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 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 2018 ; 201 (1): 134-44 Nephropedia Template TP {{tp|p=29760191|t=2018. Effects of influenza on alveolar macrophage viability are dependent on mouse genetic strain¥ |pdf=|usr=}}{{29760191}} gab.com Text Effects of influenza on alveolar macrophage viability are dependent on mouse genetic strain¥ JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=29760191 #FOAvip Secondary bacterial coinfections following influenza virus pose a serious threat to human health. Therefore, it is of significant clinical relevance to understand the immunological causes of this increased susceptibility. Influenza-induced alterations in alveolar macrophages have been shown to be a major underlying cause of the increased susceptibility to bacterial superinfection. However, the mechanisms responsible for this remain under debate, specifically, whether alveolar macrophages are depleted in response to influenza infection or are maintained post-infection, but with disrupted phagocytic activity. The data presented here resolves this issue by showing that either mechanism can differentially occur in individual mouse strains. BALB/c mice exhibited a dramatic IFN-?-dependent reduction in levels of alveolar macrophages following infection with influenza A, whereas alveolar macrophage levels in C57Bl/6 mice were maintained throughout the course of influenza infection, although the cells displayed an altered phenotype, namely an upregulation in CD11b expression. These strain differences were observed regardless of whether infection was performed with low or high doses of influenza virus. Furthermore, infection with either the H1N1 A/California/04/2009 (CA04) or H1N1 A/PR8/1934 (PR8) virus strain yielded similar results. Regardless of alveolar macrophage viability, both BALB/c and C57Bl/6 mice showed a high level of susceptibility to post-influenza bacterial infection. These findings resolve the apparent inconsistencies in the literature, identify mouse strain-dependent differences in the alveolar macrophage response to influenza infection, and ultimately, may facilitate translation of the mouse model to clinical application. Twit Text FOAVip Effects of influenza on alveolar macrophage viability are dependent on mouse genetic strain¥ ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=29760191 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29760191 #FOAvip English Wikipedia <ref>{{Cite pmid|29760191}}</ref> Effects of influenza on alveolar macrophage viability are dependent on mouse genetic strain¥ #MMPMID29760191 Califano D; Furuya Y; Metzger DW J Immunol 2018[Jul]; 201 (1): 134-44 PMID29760191show ga Secondary bacterial coinfections following influenza virus pose a serious threat to human health. Therefore, it is of significant clinical relevance to understand the immunological causes of this increased susceptibility. Influenza-induced alterations in alveolar macrophages have been shown to be a major underlying cause of the increased susceptibility to bacterial superinfection. However, the mechanisms responsible for this remain under debate, specifically, whether alveolar macrophages are depleted in response to influenza infection or are maintained post-infection, but with disrupted phagocytic activity. The data presented here resolves this issue by showing that either mechanism can differentially occur in individual mouse strains. BALB/c mice exhibited a dramatic IFN-?-dependent reduction in levels of alveolar macrophages following infection with influenza A, whereas alveolar macrophage levels in C57Bl/6 mice were maintained throughout the course of influenza infection, although the cells displayed an altered phenotype, namely an upregulation in CD11b expression. These strain differences were observed regardless of whether infection was performed with low or high doses of influenza virus. Furthermore, infection with either the H1N1 A/California/04/2009 (CA04) or H1N1 A/PR8/1934 (PR8) virus strain yielded similar results. Regardless of alveolar macrophage viability, both BALB/c and C57Bl/6 mice showed a high level of susceptibility to post-influenza bacterial infection. These findings resolve the apparent inconsistencies in the literature, identify mouse strain-dependent differences in the alveolar macrophage response to influenza infection, and ultimately, may facilitate translation of the mouse model to clinical application. äEffects of influenza on alveolar macrophage viability are dependent on(epmc).pdf DeepDyve Pubget Overpricing