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10.3390/v11060505 http://scihub22266oqcxt.onion/10.3390/v11060505 C6630660!6630660 !31159430     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=31159430 &cmd=llinks): Failed to open stream: HTTP request failed! 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Peroxisome Proliferator-Activated Receptor Gamma (PPAR?) Suppresses Inflammation and Bacterial Clearance during Influenza-Bacterial Super-Infection |pdf=|usr=}}{{31159430 }} gab.com Text Peroxisome Proliferator-Activated Receptor Gamma (PPAR ) Suppresses Inflammation and Bacterial Clearance during Influenza-Bacterial Super-Infection JO: Viruses http://www.kidney.de/pget.php?&tw=1&pmid=31159430 #FOAvip Influenza virus is among the most common causes of respiratory illness worldwide and can be complicated by secondary bacterial pneumonia, a frequent cause of mortality. When influenza virus infects the lung, the innate immune response is activated, and interferons and inflammatory mediators are released. This "cytokine storm" is thought to play a role in influenza-induced lung pathogenesis. Peroxisome proliferator-activated receptor gamma (PPAR?) is a member of the nuclear hormone receptor super-family. PPAR? has numerous functions including enhancing lipid and glucose metabolism and cellular differentiation and suppressing inflammation. Synthetic PPAR??agonists (thiazolidinediones or glitazones) have been used clinically in the treatment of type II diabetes. Using data from the National Health and Nutrition Examination Survey (NHANES), diabetic participants taking rosiglitazone had an increased risk of mortality from influenza/pneumonia compared to those not taking the drug. We examined the effect of rosiglitazone treatment during influenza and secondary bacterial (Methicillin resistant Staphylococcus aureus) pneumonia in mice. We found decreased influenza viral burden, decreased numbers of neutrophils and macrophages in bronchoalveolar lavage, and decreased production of cytokines and chemokines in influenza infected, rosiglitazone-treated mice when compared to controls. However, rosiglitazone treatment compromised bacterial clearance during influenza-bacterial super-infection. Both human and mouse data suggest that rosiglitazone treatment worsens the outcome of influenza-associated pneumonia. Twit Text FOAVip Peroxisome Proliferator-Activated Receptor Gamma (PPAR ) Suppresses Inflammation and Bacterial Clearance during Influenza-Bacterial Super-Infection ????Viruses http://www.kidney.de/pget.php?&tw=1&pmid=31159430 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=31159430 #FOAvip English Wikipedia <ref>{{Cite pmid|31159430 }}</ref> Peroxisome Proliferator-Activated Receptor Gamma (PPAR?) Suppresses Inflammation and Bacterial Clearance during Influenza-Bacterial Super-Infection #MMPMID31159430 Gopal R ; Mendy A ; Marinelli MA ; Richwalls LJ ; Seger PJ ; Patel S ; McHugh KJ ; Rich HE ; Grousd JA ; Forno E ; Alcorn JF Viruses 2019[Jun]; 11 (6 ): ä PMID31159430 show ga Influenza virus is among the most common causes of respiratory illness worldwide and can be complicated by secondary bacterial pneumonia, a frequent cause of mortality. When influenza virus infects the lung, the innate immune response is activated, and interferons and inflammatory mediators are released. This "cytokine storm" is thought to play a role in influenza-induced lung pathogenesis. Peroxisome proliferator-activated receptor gamma (PPAR?) is a member of the nuclear hormone receptor super-family. PPAR? has numerous functions including enhancing lipid and glucose metabolism and cellular differentiation and suppressing inflammation. Synthetic PPAR??agonists (thiazolidinediones or glitazones) have been used clinically in the treatment of type II diabetes. Using data from the National Health and Nutrition Examination Survey (NHANES), diabetic participants taking rosiglitazone had an increased risk of mortality from influenza/pneumonia compared to those not taking the drug. We examined the effect of rosiglitazone treatment during influenza and secondary bacterial (Methicillin resistant Staphylococcus aureus) pneumonia in mice. We found decreased influenza viral burden, decreased numbers of neutrophils and macrophages in bronchoalveolar lavage, and decreased production of cytokines and chemokines in influenza infected, rosiglitazone-treated mice when compared to controls. However, rosiglitazone treatment compromised bacterial clearance during influenza-bacterial super-infection. Both human and mouse data suggest that rosiglitazone treatment worsens the outcome of influenza-associated pneumonia. |*Bacterial Infections/complications/drug therapy/immunology [MESH] |*Influenza, Human/complications/drug therapy/immunology [MESH] |Animals [MESH] |Coinfection/*drug therapy/immunology/microbiology/virology [MESH] |Cytokines/drug effects/metabolism [MESH] |Diabetes Mellitus, Type 2/complications/drug therapy/microbiology/virology [MESH] |Female [MESH] |Gene Expression Regulation/drug effects [MESH] |Humans [MESH] |Inflammation/genetics/microbiology/*pathology/virology [MESH] |Influenza A Virus, H1N1 Subtype/drug effects/growth & development/immunology [MESH] |Interferons/drug effects/metabolism [MESH] |Lung/immunology/microbiology/pathology/virology [MESH] |Male [MESH] |Methicillin-Resistant Staphylococcus aureus/drug effects/growth & development/immunology [MESH] |Mice [MESH] |PPAR gamma/agonists [MESH] |Rosiglitazone/*adverse effects/pharmacology [MESH] |Signal Transduction/drug effects [MESH]Peroxisome Proliferator-Activated Receptor Gamma (PPAR?) 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