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10.3389/fimmu.2018.00975 http://scihub22266oqcxt.onion/10.3389/fimmu.2018.00975 C5962662!5962662 !29867955     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29867955 &cmd=llinks): Failed to open stream: HTTP request failed! 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Phosphatidyl Inositol 3 Kinase-Gamma Balances Antiviral and Inflammatory Responses During Influenza A H1N1 Infection: From Murine Model to Genetic Association in Patients |pdf=|usr=}}{{29867955 }} gab.com Text Phosphatidyl Inositol 3 Kinase-Gamma Balances Antiviral and Inflammatory Responses During Influenza A H1N1 Infection: From Murine Model to Genetic Association in Patients JO: Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=29867955 #FOAvip Influenza A virus (IAV) infection causes severe pulmonary disease characterized by intense leukocyte infiltration. Phosphoinositide-3 kinases (PI3Ks) are central signaling enzymes, involved in cell growth, survival, and migration. Class IB PI3K or phosphatidyl inositol 3 kinase-gamma (PI3K?), mainly expressed by leukocytes, is involved in cell migration during inflammation. Here, we investigated the contribution of PI3K? for the inflammatory and antiviral responses to IAV. PI3K? knockout (KO) mice were highly susceptible to lethality following infection with influenza A/WSN/33 H1N1. In the early time points of infection, infiltration of neutrophils was higher than WT mice whereas type-I and type-III IFN expression and p38 activation were reduced in PI3K? KO mice resulting in higher viral loads when compared with WT mice. Blockade of p38 in WT macrophages infected with IAV reduced levels of interferon-stimulated gene 15 protein to those induced in PI3K? KO macrophages, suggesting that p38 is downstream of antiviral responses mediated by PI3K?. PI3K? KO-derived fibroblasts or macrophages showed reduced type-I IFN transcription and altered pro-inflammatory cytokines suggesting a cell autonomous imbalance between inflammatory and antiviral responses. Seven days after IAV infection, there were reduced infiltration of natural killer cells and CD8(+) T lymphocytes, increased concentration of inflammatory cytokines in bronchoalveolar fluid, reduced numbers of resolving macrophages, and IL-10 levels in PI3K? KO. This imbalanced environment in PI3K? KO-infected mice culminated in enhanced lung neutrophil infiltration, reactive oxygen species release, and lung damage that together with the increased viral loads, contributed to higher mortality in PI3K? KO mice compared with WT mice. In humans, we tested the genetic association of disease severity in influenza A/H1N1pdm09-infected patients with three potentially functional PIK3CG single-nucleotide polymorphisms (SNPs), rs1129293, rs17847825, and rs2230460. We observed that SNPs rs17847825 and rs2230460 (A and T alleles, respectively) were significantly associated with protection from severe disease using the recessive model in patients infected with influenza A(H1N1)pdm09. Altogether, our results suggest that PI3K? is crucial in balancing antiviral and inflammatory responses to IAV infection. Twit Text FOAVip Phosphatidyl Inositol 3 Kinase-Gamma Balances Antiviral and Inflammatory Responses During Influenza A H1N1 Infection: From Murine Model to Genetic Association in Patients ????Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=29867955 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29867955 #FOAvip English Wikipedia <ref>{{Cite pmid|29867955 }}</ref> Phosphatidyl Inositol 3 Kinase-Gamma Balances Antiviral and Inflammatory Responses During Influenza A H1N1 Infection: From Murine Model to Genetic Association in Patients #MMPMID29867955 Garcia CC ; Tavares LP ; Dias ACF ; Kehdy F ; Alvarado-Arnez LE ; Queiroz-Junior CM ; Galvão I ; Lima BH ; Matos AR ; Gonçalves APF ; Soriani FM ; Moraes MO ; Marques JT ; Siqueira MM ; Machado AMV ; Sousa LP ; Russo RC ; Teixeira MM Front Immunol 2018[]; 9 (ä): 975 PMID29867955 show ga Influenza A virus (IAV) infection causes severe pulmonary disease characterized by intense leukocyte infiltration. Phosphoinositide-3 kinases (PI3Ks) are central signaling enzymes, involved in cell growth, survival, and migration. Class IB PI3K or phosphatidyl inositol 3 kinase-gamma (PI3K?), mainly expressed by leukocytes, is involved in cell migration during inflammation. Here, we investigated the contribution of PI3K? for the inflammatory and antiviral responses to IAV. PI3K? knockout (KO) mice were highly susceptible to lethality following infection with influenza A/WSN/33 H1N1. In the early time points of infection, infiltration of neutrophils was higher than WT mice whereas type-I and type-III IFN expression and p38 activation were reduced in PI3K? KO mice resulting in higher viral loads when compared with WT mice. Blockade of p38 in WT macrophages infected with IAV reduced levels of interferon-stimulated gene 15 protein to those induced in PI3K? KO macrophages, suggesting that p38 is downstream of antiviral responses mediated by PI3K?. PI3K? KO-derived fibroblasts or macrophages showed reduced type-I IFN transcription and altered pro-inflammatory cytokines suggesting a cell autonomous imbalance between inflammatory and antiviral responses. Seven days after IAV infection, there were reduced infiltration of natural killer cells and CD8(+) T lymphocytes, increased concentration of inflammatory cytokines in bronchoalveolar fluid, reduced numbers of resolving macrophages, and IL-10 levels in PI3K? KO. This imbalanced environment in PI3K? KO-infected mice culminated in enhanced lung neutrophil infiltration, reactive oxygen species release, and lung damage that together with the increased viral loads, contributed to higher mortality in PI3K? KO mice compared with WT mice. In humans, we tested the genetic association of disease severity in influenza A/H1N1pdm09-infected patients with three potentially functional PIK3CG single-nucleotide polymorphisms (SNPs), rs1129293, rs17847825, and rs2230460. We observed that SNPs rs17847825 and rs2230460 (A and T alleles, respectively) were significantly associated with protection from severe disease using the recessive model in patients infected with influenza A(H1N1)pdm09. Altogether, our results suggest that PI3K? is crucial in balancing antiviral and inflammatory responses to IAV infection. |*Inflammation [MESH] |Adolescent [MESH] |Adult [MESH] |Animals [MESH] |Antiviral Agents [MESH] |CD8-Positive T-Lymphocytes/immunology [MESH] |Class Ib Phosphatidylinositol 3-Kinase/*genetics/immunology [MESH] |Cytokines/immunology [MESH] |Disease Models, Animal [MESH] |Female [MESH] |Genetic Association Studies [MESH] |Humans [MESH] |Influenza A Virus, H1N1 Subtype [MESH] |Influenza, Human/*immunology [MESH] |MAP Kinase Signaling System [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |Middle Aged [MESH] |Neutrophil Infiltration [MESH] |Orthomyxoviridae Infections/*immunology [MESH] |Polymorphism, Single Nucleotide [MESH]Phosphatidyl Inositol 3 Kinase-Gamma Balances Antiviral and Inflammato(epmc).pdf DeepDyve Pubget Overpricing