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10.1186/cc13171 http://scihub22266oqcxt.onion/10.1186/cc13171 C4057515!4057515 !24373231     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24373231 &cmd=llinks): Failed to open stream: HTTP request failed! 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Inhibition of the inflammatory cytokine tumor necrosis factor-alpha with etanercept provides protection against lethal H1N1 influenza infection in mice |pdf=|usr=}}{{24373231 }} gab.com Text Inhibition of the inflammatory cytokine tumor necrosis factor-alpha with etanercept provides protection against lethal H1N1 influenza infection in mice JO: Crit Care http://www.kidney.de/pget.php?&tw=1&pmid=24373231 #FOAvip INTRODUCTION: Factors implicated in influenza-mediated morbidity and mortality include robust cytokine production (cytokine storm), excessive inflammatory infiltrates, and virus-induced tissue destruction. Tumor necrosis factor-alpha (TNF-?) is an important pro-inflammatory cytokine present during influenza infection, but it is unclear whether direct inhibition of TNF-? can elicit protection against influenza infection. METHODS: In this study, the commercially available TNF-? inhibitor etanercept was used to inhibit TNF-? induced by lethal A/FM/1/47 (H1N1) influenza virus infection of mice. The effects of TNF-? inhibition on mouse survival, pathologic changes, immune cell infiltration, inflammatory cytokine secretion, Toll-like receptor expression, and activation of the NF-?B (nuclear factor kappa B) signaling pathway were evaluated. RESULTS: The intranasal delivery of etanercept provided significant protection against mortality (30% of mice survived up to 14 days after infection) in mice treated with etanercept. In contrast, no survivors were found beyond 6 days in mice treated with saline after lethal challenge with H1N1 influenza virus. It was observed that etanercept significantly reduced inflammatory cell infiltration (for example, macrophages and neutrophils), inflammatory cytokine secretion (for example, interleukin-6, TNF-?, and interferon gamma), and expression of Toll-like receptors (TLR-3, TLR-4, and TLR-7). Etanercept also downregulated and inhibited the cascade proteins of the NF-?B signaling pathway (for example, MyD88, TRIF, NF-?B, and p65), as well as enhanced host control of virus replication. CONCLUSIONS: These findings indicate that etanercept, by blocking TNF-?, can significantly downregulate excessive inflammatory immune responses and provide protection against lethal influenza infection, making its use a novel strategy for controlling severe influenza-induced viral pneumonia. Twit Text FOAVip Inhibition of the inflammatory cytokine tumor necrosis factor-alpha with etanercept provides protection against lethal H1N1 influenza infection in mice ????Crit Care http://www.kidney.de/pget.php?&tw=1&pmid=24373231 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24373231 #FOAvip English Wikipedia <ref>{{Cite pmid|24373231 }}</ref> Inhibition of the inflammatory cytokine tumor necrosis factor-alpha with etanercept provides protection against lethal H1N1 influenza infection in mice #MMPMID24373231 Shi X ; Zhou W ; Huang H ; Zhu H ; Zhou P ; Zhu H ; Ju D Crit Care 2013[Dec]; 17 (6 ): R301 PMID24373231 show ga INTRODUCTION: Factors implicated in influenza-mediated morbidity and mortality include robust cytokine production (cytokine storm), excessive inflammatory infiltrates, and virus-induced tissue destruction. Tumor necrosis factor-alpha (TNF-?) is an important pro-inflammatory cytokine present during influenza infection, but it is unclear whether direct inhibition of TNF-? can elicit protection against influenza infection. METHODS: In this study, the commercially available TNF-? inhibitor etanercept was used to inhibit TNF-? induced by lethal A/FM/1/47 (H1N1) influenza virus infection of mice. The effects of TNF-? inhibition on mouse survival, pathologic changes, immune cell infiltration, inflammatory cytokine secretion, Toll-like receptor expression, and activation of the NF-?B (nuclear factor kappa B) signaling pathway were evaluated. RESULTS: The intranasal delivery of etanercept provided significant protection against mortality (30% of mice survived up to 14 days after infection) in mice treated with etanercept. In contrast, no survivors were found beyond 6 days in mice treated with saline after lethal challenge with H1N1 influenza virus. It was observed that etanercept significantly reduced inflammatory cell infiltration (for example, macrophages and neutrophils), inflammatory cytokine secretion (for example, interleukin-6, TNF-?, and interferon gamma), and expression of Toll-like receptors (TLR-3, TLR-4, and TLR-7). Etanercept also downregulated and inhibited the cascade proteins of the NF-?B signaling pathway (for example, MyD88, TRIF, NF-?B, and p65), as well as enhanced host control of virus replication. CONCLUSIONS: These findings indicate that etanercept, by blocking TNF-?, can significantly downregulate excessive inflammatory immune responses and provide protection against lethal influenza infection, making its use a novel strategy for controlling severe influenza-induced viral pneumonia. |*Influenza A Virus, H1N1 Subtype [MESH] |Animals [MESH] |Antiviral Agents/*therapeutic use [MESH] |Cytokines/metabolism [MESH] |Down-Regulation [MESH] |Etanercept [MESH] |Immunity, Innate [MESH] |Immunoglobulin G/*therapeutic use [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred BALB C [MESH] |NF-kappa B/metabolism [MESH] |Orthomyxoviridae Infections/*drug therapy/immunology/pathology [MESH] |Pneumonia, Viral/*drug therapy/immunology/pathology [MESH] |RNA, Messenger/metabolism [MESH] |Receptors, Tumor Necrosis Factor/*therapeutic use [MESH] |Signal Transduction [MESH] |Toll-Like Receptors/metabolism [MESH] |Tumor Necrosis Factor-alpha/*antagonists & inhibitors [MESH]Inhibition of the inflammatory cytokine tumor necrosis factor-alpha wi(epmc).pdf DeepDyve Pubget Overpricing