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10.1038/s41564-019-0444-3 http://scihub22266oqcxt.onion/10.1038/s41564-019-0444-3 31110361!ä!31110361 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Microbiol 2019 ; 4 (8): 1389-1400 Nephropedia Template TP {{tp|p=31110361|t=2019. Leukotriene B(4)-type I interferon axis regulates macrophage-mediated disease tolerance to influenza infection |pdf=|usr=}}{{31110361}} gab.com Text Leukotriene B(4)-type I interferon axis regulates macrophage-mediated disease tolerance to influenza infection JO: Nat Microbiol http://www.kidney.de/pget.php?&tw=1&pmid=31110361 #FOAvip Host defence against influenza A virus (IAV) infection depends not only on host resistance to eliminate the virus, but also disease tolerance to limit lung tissue damage and maintain pulmonary function. Fatal IAV infections are frequently the result of a maladaptive immune response that compromises disease tolerance rather than host resistance to infection. Here, we show that the leukotriene B(4) (LTB(4))-type I interferon (IFN) axis promotes a distinct mechanism of disease tolerance to pulmonary IAV infection. We demonstrate that mice genetically deficient in LTB(4) signalling (Blt1R(-/-)) are more susceptible to IAV infection compared to control mice, despite similar pulmonary viral loads. The increased susceptibility of Blt1R(-/-) mice is associated with an accumulation of inflammatory monocyte-derived macrophages (IMMs) causing increased lung immunopathology. We mechanistically define that LTB(4) signalling via the BLT1 receptor enhances the activation of the type I IFN-alpha/beta receptor (IFNAR)/ and signal transducer and activator of transcription 1 (STAT1), which leads to IFN-alpha production by interstitial macrophages to suppresse in situ IMM proliferation. Importantly, the delivery of a single dose of LTB(4) at the peak viral load reduces IMM proliferation, controls tissue damage and increases survival without affecting host resistance to IAV. These results reveal an unexpected anti-inflammatory role of LTB(4) in disease tolerance to IAV infection. Twit Text FOAVip Leukotriene B(4)-type I interferon axis regulates macrophage-mediated disease tolerance to influenza infection ????Nat Microbiol http://www.kidney.de/pget.php?&tw=1&pmid=31110361 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=31110361 #FOAvip English Wikipedia <ref>{{Cite pmid|31110361}}</ref> Leukotriene B(4)-type I interferon axis regulates macrophage-mediated disease tolerance to influenza infection #MMPMID31110361 Pernet E; Downey J; Vinh DC; Powell WS; Divangahi M Nat Microbiol 2019[Aug]; 4 (8): 1389-1400 PMID31110361show ga Host defence against influenza A virus (IAV) infection depends not only on host resistance to eliminate the virus, but also disease tolerance to limit lung tissue damage and maintain pulmonary function. Fatal IAV infections are frequently the result of a maladaptive immune response that compromises disease tolerance rather than host resistance to infection. Here, we show that the leukotriene B(4) (LTB(4))-type I interferon (IFN) axis promotes a distinct mechanism of disease tolerance to pulmonary IAV infection. We demonstrate that mice genetically deficient in LTB(4) signalling (Blt1R(-/-)) are more susceptible to IAV infection compared to control mice, despite similar pulmonary viral loads. The increased susceptibility of Blt1R(-/-) mice is associated with an accumulation of inflammatory monocyte-derived macrophages (IMMs) causing increased lung immunopathology. We mechanistically define that LTB(4) signalling via the BLT1 receptor enhances the activation of the type I IFN-alpha/beta receptor (IFNAR)/ and signal transducer and activator of transcription 1 (STAT1), which leads to IFN-alpha production by interstitial macrophages to suppresse in situ IMM proliferation. Importantly, the delivery of a single dose of LTB(4) at the peak viral load reduces IMM proliferation, controls tissue damage and increases survival without affecting host resistance to IAV. These results reveal an unexpected anti-inflammatory role of LTB(4) in disease tolerance to IAV infection. |*Immune Tolerance[MESH] |Animals[MESH] |Cell Death[MESH] |Cell Line[MESH] |Cell Proliferation[MESH] |Humans[MESH] |Immunity, Innate/*immunology[MESH] |Influenza A virus/immunology[MESH] |Influenza, Human/*immunology/pathology[MESH] |Interferon Type I/*metabolism[MESH] |Leukotriene B4/*metabolism[MESH] |Lung/immunology/pathology[MESH] |Macrophages/*metabolism[MESH] |Mice[MESH] |Mice, Inbred C57BL[MESH] |Mice, Knockout[MESH] |Orthomyxoviridae Infections/immunology[MESH] |Receptor, Interferon alpha-beta/genetics/metabolism[MESH] |Receptors, CCR2/genetics[MESH] |STAT1 Transcription Factor/metabolism[MESH]Leukotriene B(4)-type I interferon axis regulates macrophage-mediated (epmc).pdf DeepDyve Pubget Overpricing