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10.1089/vim.2019.0016 http://scihub22266oqcxt.onion/10.1089/vim.2019.0016 C6534095!6534095 !31009317     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=31009317 &cmd=llinks): Failed to open stream: HTTP request failed! 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Targeting Peroxisome Proliferator-Activated Receptor-Gamma Decreases Host Mortality After Influenza Infection in Obese Mice |pdf=|usr=}}{{31009317 }} gab.com Text Targeting Peroxisome Proliferator-Activated Receptor-Gamma Decreases Host Mortality After Influenza Infection in Obese Mice JO: Viral Immunol http://www.kidney.de/pget.php?&tw=1&pmid=31009317 #FOAvip Obesity is an independent risk factor for severe influenza infection. However, the underlying cellular and molecular mechanisms are still incompletely understood. In this study, we have utilized a murine influenza infection model in genetic-induced obese (db/db) mice to explore the mechanisms by which obesity increases host susceptibility to influenza infection. We find that db/db mice have enhanced viral replication, exaggerated inflammatory responses, and dysregulated lung repair process after influenza infection, and consequently increased host mortality. Furthermore, we demonstrate that the transcription factor peroxisome proliferator-activated receptor-gamma (PPAR-?), an important inflammation regulator, was downregulated in the lung macrophages of db/db mice after influenza infection. Strikingly, the treatment of 15-deoxy-?12, 14-prostaglandin J2 (15d-PGJ2), a PPAR-? agonist, largely rescued the survival of db/db mice after influenza infection. Interestingly, macrophage PPAR-?-deficient mice exhibited enhanced mortality after influenza infection and 15d-PGJ2 fails to rescue host mortality in macrophage PPAR-?-deficient mice, suggesting that PPAR-? expression in macrophages is critical for the action of 15d-PGJ2. These data indicate that obesity attenuates lung antiviral immunity and hampers host recovery through the modulation of macrophage PPAR-? expression. Furthermore, modalities targeting macrophage PPAR-? expression and/or function may serve as promising therapeutics to treat severe influenza infection in obese patients. Twit Text FOAVip Targeting Peroxisome Proliferator-Activated Receptor-Gamma Decreases Host Mortality After Influenza Infection in Obese Mice ????Viral Immunol http://www.kidney.de/pget.php?&tw=1&pmid=31009317 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=31009317 #FOAvip English Wikipedia <ref>{{Cite pmid|31009317 }}</ref> Targeting Peroxisome Proliferator-Activated Receptor-Gamma Decreases Host Mortality After Influenza Infection in Obese Mice #MMPMID31009317 Huang S ; Jiang L ; Cheon IS ; Sun J Viral Immunol 2019[May]; 32 (4 ): 161-169 PMID31009317 show ga Obesity is an independent risk factor for severe influenza infection. However, the underlying cellular and molecular mechanisms are still incompletely understood. In this study, we have utilized a murine influenza infection model in genetic-induced obese (db/db) mice to explore the mechanisms by which obesity increases host susceptibility to influenza infection. We find that db/db mice have enhanced viral replication, exaggerated inflammatory responses, and dysregulated lung repair process after influenza infection, and consequently increased host mortality. Furthermore, we demonstrate that the transcription factor peroxisome proliferator-activated receptor-gamma (PPAR-?), an important inflammation regulator, was downregulated in the lung macrophages of db/db mice after influenza infection. Strikingly, the treatment of 15-deoxy-?12, 14-prostaglandin J2 (15d-PGJ2), a PPAR-? agonist, largely rescued the survival of db/db mice after influenza infection. Interestingly, macrophage PPAR-?-deficient mice exhibited enhanced mortality after influenza infection and 15d-PGJ2 fails to rescue host mortality in macrophage PPAR-?-deficient mice, suggesting that PPAR-? expression in macrophages is critical for the action of 15d-PGJ2. These data indicate that obesity attenuates lung antiviral immunity and hampers host recovery through the modulation of macrophage PPAR-? expression. Furthermore, modalities targeting macrophage PPAR-? expression and/or function may serve as promising therapeutics to treat severe influenza infection in obese patients. |*Down-Regulation [MESH] |Animals [MESH] |Disease Models, Animal [MESH] |Immunity, Innate [MESH] |Immunologic Factors/agonists/*biosynthesis [MESH] |Inflammation/pathology [MESH] |Lung/pathology [MESH] |Macrophages/immunology [MESH] |Mice, Obese [MESH] |Obesity/*complications [MESH] |Orthomyxoviridae Infections/*pathology [MESH] |Orthomyxoviridae/growth & development [MESH] |PPAR gamma/agonists/*biosynthesis [MESH]Targeting Peroxisome Proliferator-Activated Receptor-Gamma Decreases H(epmc).pdf DeepDyve Pubget Overpricing