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10.1073/pnas.1902310116 http://scihub22266oqcxt.onion/10.1073/pnas.1902310116 C6575592!6575592 !31138703     free     free     free 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 Deprecated: Implicit conversion from float 247.2 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 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\31138703 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Proc+Natl+Acad+Sci+U+S+A 2019 ; 116 (24 ): 11888-11893 Nephropedia Template TP {{tp|p=31138703 |t=2019. BCL6 modulates tissue neutrophil survival and exacerbates pulmonary inflammation following influenza virus infection |pdf=|usr=}}{{31138703 }} gab.com Text BCL6 modulates tissue neutrophil survival and exacerbates pulmonary inflammation following influenza virus infection JO: Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=31138703 #FOAvip Neutrophils are vital for antimicrobial defense; however, their role during viral infection is less clear. Furthermore, the molecular regulation of neutrophil fate and function at the viral infected sites is largely elusive. Here we report that BCL6 deficiency in myeloid cells exhibited drastically enhanced host resistance to severe influenza A virus (IAV) infection. In contrast to the notion that BCL6 functions to suppress innate inflammation, we find that myeloid BCL6 deficiency diminished lung inflammation without affecting viral loads. Using a series of Cre-transgenic, reporter, and knockout mouse lines, we demonstrate that BCL6 deficiency in neutrophils, but not in monocytes or lung macrophages, attenuated host inflammation and morbidity following IAV infection. Mechanistically, BCL6 bound to the neutrophil gene loci involved in cellular apoptosis in cells specifically at the site of infection. As such, BCL6 disruption resulted in increased expression of apoptotic genes in neutrophils in the respiratory tract, but not in the circulation or bone marrow. Consequently, BCL6 deficiency promoted tissue neutrophil apoptosis. Partial neutrophil depletion led to diminished pulmonary inflammation and decreased host morbidity. Our results reveal a previously unappreciated role of BCL6 in modulating neutrophil apoptosis at the site of infection for the regulation of host disease development following viral infection. Furthermore, our studies indicate that tissue-specific regulation of neutrophil survival modulates host inflammation and tissue immunopathology during acute respiratory viral infection. Twit Text FOAVip BCL6 modulates tissue neutrophil survival and exacerbates pulmonary inflammation following influenza virus infection ????Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=31138703 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=31138703 #FOAvip English Wikipedia <ref>{{Cite pmid|31138703 }}</ref> BCL6 modulates tissue neutrophil survival and exacerbates pulmonary inflammation following influenza virus infection #MMPMID31138703 Zhu B ; Zhang R ; Li C ; Jiang L ; Xiang M ; Ye Z ; Kita H ; Melnick AM ; Dent AL ; Sun J Proc Natl Acad Sci U S A 2019[Jun]; 116 (24 ): 11888-11893 PMID31138703 show ga Neutrophils are vital for antimicrobial defense; however, their role during viral infection is less clear. Furthermore, the molecular regulation of neutrophil fate and function at the viral infected sites is largely elusive. Here we report that BCL6 deficiency in myeloid cells exhibited drastically enhanced host resistance to severe influenza A virus (IAV) infection. In contrast to the notion that BCL6 functions to suppress innate inflammation, we find that myeloid BCL6 deficiency diminished lung inflammation without affecting viral loads. Using a series of Cre-transgenic, reporter, and knockout mouse lines, we demonstrate that BCL6 deficiency in neutrophils, but not in monocytes or lung macrophages, attenuated host inflammation and morbidity following IAV infection. Mechanistically, BCL6 bound to the neutrophil gene loci involved in cellular apoptosis in cells specifically at the site of infection. As such, BCL6 disruption resulted in increased expression of apoptotic genes in neutrophils in the respiratory tract, but not in the circulation or bone marrow. Consequently, BCL6 deficiency promoted tissue neutrophil apoptosis. Partial neutrophil depletion led to diminished pulmonary inflammation and decreased host morbidity. Our results reveal a previously unappreciated role of BCL6 in modulating neutrophil apoptosis at the site of infection for the regulation of host disease development following viral infection. Furthermore, our studies indicate that tissue-specific regulation of neutrophil survival modulates host inflammation and tissue immunopathology during acute respiratory viral infection. |Animals [MESH] |Apoptosis/physiology [MESH] |Host-Pathogen Interactions/physiology [MESH] |Influenza A virus/*pathogenicity [MESH] |Lung/metabolism/virology [MESH] |Macrophages, Alveolar/metabolism/virology [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |Neutrophil Infiltration/physiology [MESH] |Neutrophils/*metabolism/virology [MESH] |Orthomyxoviridae Infections/*metabolism [MESH] |Pneumonia/*metabolism/virology [MESH] |Proto-Oncogene Proteins c-bcl-6/*metabolism [MESH]BCL6 modulates tissue neutrophil survival and exacerbates pulmonary in(epmc).pdf DeepDyve Pubget Overpricing