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10.1128/JVI.00030-19 http://scihub22266oqcxt.onion/10.1128/JVI.00030-19 C6475778!6475778 !30787149     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 269.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 269.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 269.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 269.2 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\30787149 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Virol 2019 ; 93 (9 ): ä Nephropedia Template TP {{tp|p=30787149 |t=2019. PPAR-? in Macrophages Limits Pulmonary Inflammation and Promotes Host Recovery following Respiratory Viral Infection |pdf=|usr=}}{{30787149 }} gab.com Text PPAR- in Macrophages Limits Pulmonary Inflammation and Promotes Host Recovery following Respiratory Viral Infection JO: J Virol http://www.kidney.de/pget.php?&tw=1&pmid=30787149 #FOAvip Alveolar macrophages (AM) play pivotal roles in modulating host defense, pulmonary inflammation, and tissue injury following respiratory viral infections. However, the transcriptional regulation of AM function during respiratory viral infections is still largely undefined. Here we have screened the expression of 84 transcription factors in AM in response to influenza A virus (IAV) infection. We found that the transcription factor PPAR-? was downregulated following IAV infection in AM through type I interferon (IFN)-dependent signaling. PPAR-? expression in AM was critical for the suppression of exaggerated antiviral and inflammatory responses of AM following IAV and respiratory syncytial virus (RSV) infections. Myeloid PPAR-? deficiency resulted in enhanced host morbidity and increased pulmonary inflammation following both IAV and RSV infections, suggesting that macrophage PPAR-? is vital for restricting severe host disease development. Using approaches to selectively deplete recruiting monocytes, we demonstrate that PPAR-? expression in resident AM is likely important in regulating host disease development. Furthermore, we show that PPAR-? was critical for the expression of wound healing genes in AM. As such, myeloid PPAR-? deficiency resulted in impaired inflammation resolution and defective tissue repair following IAV infection. Our data suggest a critical role of PPAR-? expression in lung macrophages in the modulation of pulmonary inflammation, the development of acute host diseases, and the proper restoration of tissue homeostasis following respiratory viral infections.IMPORTANCE Respiratory viral infections, like IAV and respiratory syncytial virus (RSV) infections, impose great challenges to public health. Alveolar macrophages (AM) are lung-resident immune cells that play important roles in protecting the host against IAV and RSV infections. However, the underlying molecular mechanisms by which AM modulate host inflammation, disease development, and tissue recovery are not very well understood. Here we identify that PPAR-? expression in AM is crucial to suppress pulmonary inflammation and diseases and to promote fast host recovery from IAV and RSV infections. Our data suggest that targeting macrophage PPAR-? may be a promising therapeutic option in the future to suppress acute inflammation and simultaneously promote recovery from severe diseases associated with respiratory viral infections. Twit Text FOAVip PPAR- in Macrophages Limits Pulmonary Inflammation and Promotes Host Recovery following Respiratory Viral Infection ????J Virol http://www.kidney.de/pget.php?&tw=1&pmid=30787149 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30787149 #FOAvip English Wikipedia <ref>{{Cite pmid|30787149 }}</ref> PPAR-? in Macrophages Limits Pulmonary Inflammation and Promotes Host Recovery following Respiratory Viral Infection #MMPMID30787149 Huang S ; Zhu B ; Cheon IS ; Goplen NP ; Jiang L ; Zhang R ; Peebles RS ; Mack M ; Kaplan MH ; Limper AH ; Sun J J Virol 2019[May]; 93 (9 ): ä PMID30787149 show ga Alveolar macrophages (AM) play pivotal roles in modulating host defense, pulmonary inflammation, and tissue injury following respiratory viral infections. However, the transcriptional regulation of AM function during respiratory viral infections is still largely undefined. Here we have screened the expression of 84 transcription factors in AM in response to influenza A virus (IAV) infection. We found that the transcription factor PPAR-? was downregulated following IAV infection in AM through type I interferon (IFN)-dependent signaling. PPAR-? expression in AM was critical for the suppression of exaggerated antiviral and inflammatory responses of AM following IAV and respiratory syncytial virus (RSV) infections. Myeloid PPAR-? deficiency resulted in enhanced host morbidity and increased pulmonary inflammation following both IAV and RSV infections, suggesting that macrophage PPAR-? is vital for restricting severe host disease development. Using approaches to selectively deplete recruiting monocytes, we demonstrate that PPAR-? expression in resident AM is likely important in regulating host disease development. Furthermore, we show that PPAR-? was critical for the expression of wound healing genes in AM. As such, myeloid PPAR-? deficiency resulted in impaired inflammation resolution and defective tissue repair following IAV infection. Our data suggest a critical role of PPAR-? expression in lung macrophages in the modulation of pulmonary inflammation, the development of acute host diseases, and the proper restoration of tissue homeostasis following respiratory viral infections.IMPORTANCE Respiratory viral infections, like IAV and respiratory syncytial virus (RSV) infections, impose great challenges to public health. Alveolar macrophages (AM) are lung-resident immune cells that play important roles in protecting the host against IAV and RSV infections. However, the underlying molecular mechanisms by which AM modulate host inflammation, disease development, and tissue recovery are not very well understood. Here we identify that PPAR-? expression in AM is crucial to suppress pulmonary inflammation and diseases and to promote fast host recovery from IAV and RSV infections. Our data suggest that targeting macrophage PPAR-? may be a promising therapeutic option in the future to suppress acute inflammation and simultaneously promote recovery from severe diseases associated with respiratory viral infections. |Animals [MESH] |Gene Expression Regulation [MESH] |Inflammation/genetics/metabolism/pathology/virology [MESH] |Influenza A virus/*metabolism [MESH] |Macrophages, Alveolar/*metabolism/pathology/virology [MESH] |Mice [MESH] |Mice, Knockout [MESH] |Orthomyxoviridae Infections/genetics/*metabolism/pathology [MESH] |PPAR gamma/*biosynthesis/genetics [MESH] |Pneumonia, Viral/genetics/*metabolism/pathology [MESH] |Respiratory Syncytial Virus Infections/genetics/*metabolism/pathology [MESH]PPAR-? in Macrophages Limits Pulmonary Inflammation and Promotes Host (epmc).pdf DeepDyve Pubget Overpricing