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10.1038/mi.2016.107 http://scihub22266oqcxt.onion/10.1038/mi.2016.107 C5471142!5471142 !27966554     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27966554 &cmd=llinks): Failed to open stream: HTTP request failed! 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IL-36 receptor deletion attenuates lung injury and decreases mortality in murine influenza pneumonia |pdf=|usr=}}{{27966554 }} gab.com Text IL-36 receptor deletion attenuates lung injury and decreases mortality in murine influenza pneumonia JO: Mucosal Immunol http://www.kidney.de/pget.php?&tw=1&pmid=27966554 #FOAvip Influenza virus causes a respiratory disease in humans that can progress to lung injury with fatal outcome. The interleukin (IL)-36 cytokines are newly described IL-1 family cytokines that promote inflammatory responses via binding to the IL-36 receptor (IL-36R). The mechanism of expression and the role of IL-36 cytokines are poorly understood. Here, we investigated the role of IL-36 cytokines in modulating the innate inflammatory response during influenza virus-induced pneumonia in mice. The intranasal administration of influenza virus upregulated IL-36? mRNA and protein production in the lungs. In vitro, influenza virus-mediated IL-36? but not IL-36? is induced and secreted from alveolar epithelial cells (AECs) through both a caspase-1 and caspase-3/7 dependent pathway. IL-36? was detected in microparticles shed from AECs and promoted the production of pro-inflammatory cytokines and chemokines in respiratory cells. IL-36R-deficient mice were protected from influenza virus-induced lung injury and mortality. Decreased mortality was associated with significantly reduced early accumulation of neutrophils and monocytes/macrophages, activation of lymphocytes, production of pro-inflammatory cytokines and chemokines, and permeability of the alveolar-epithelial barrier in despite impaired viral clearance. Taken together, these data indicate that IL-36 ligands exacerbate lung injury during influenza virus infection. Twit Text FOAVip IL-36 receptor deletion attenuates lung injury and decreases mortality in murine influenza pneumonia ????Mucosal Immunol http://www.kidney.de/pget.php?&tw=1&pmid=27966554 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27966554 #FOAvip English Wikipedia <ref>{{Cite pmid|27966554 }}</ref> IL-36 receptor deletion attenuates lung injury and decreases mortality in murine influenza pneumonia #MMPMID27966554 Aoyagi T ; Newstead MW ; Zeng X ; Kunkel SL ; Kaku M ; Standiford TJ Mucosal Immunol 2017[Jul]; 10 (4 ): 1043-1055 PMID27966554 show ga Influenza virus causes a respiratory disease in humans that can progress to lung injury with fatal outcome. The interleukin (IL)-36 cytokines are newly described IL-1 family cytokines that promote inflammatory responses via binding to the IL-36 receptor (IL-36R). The mechanism of expression and the role of IL-36 cytokines are poorly understood. Here, we investigated the role of IL-36 cytokines in modulating the innate inflammatory response during influenza virus-induced pneumonia in mice. The intranasal administration of influenza virus upregulated IL-36? mRNA and protein production in the lungs. In vitro, influenza virus-mediated IL-36? but not IL-36? is induced and secreted from alveolar epithelial cells (AECs) through both a caspase-1 and caspase-3/7 dependent pathway. IL-36? was detected in microparticles shed from AECs and promoted the production of pro-inflammatory cytokines and chemokines in respiratory cells. IL-36R-deficient mice were protected from influenza virus-induced lung injury and mortality. Decreased mortality was associated with significantly reduced early accumulation of neutrophils and monocytes/macrophages, activation of lymphocytes, production of pro-inflammatory cytokines and chemokines, and permeability of the alveolar-epithelial barrier in despite impaired viral clearance. Taken together, these data indicate that IL-36 ligands exacerbate lung injury during influenza virus infection. |Alveolar Epithelial Cells/immunology/*metabolism/virology [MESH] |Animals [MESH] |Cell-Derived Microparticles/metabolism [MESH] |Cells, Cultured [MESH] |Cytokines/metabolism [MESH] |Humans [MESH] |Immunity, Innate [MESH] |Inflammation Mediators/metabolism [MESH] |Influenza A Virus, H1N1 Subtype/*physiology [MESH] |Influenza, Human/immunology [MESH] |Interleukin-1/metabolism [MESH] |Lung Injury/*immunology [MESH] |Lung/metabolism/*pathology [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |Neutrophils/*immunology [MESH] |Orthomyxoviridae Infections/*immunology [MESH] |Receptors, Interleukin-1/genetics/*metabolism [MESH]IL-36 receptor deletion attenuates lung injury and decreases mortality(epmc).pdf DeepDyve Pubget Overpricing