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10.1084/jem.20150632 http://scihub22266oqcxt.onion/10.1084/jem.20150632 C4612096!4612096 !26392224     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26392224 &cmd=llinks): Failed to open stream: HTTP request failed! 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Critical role of phospholipase A2 group IID in age-related susceptibility to severe acute respiratory syndrome-CoV infection |pdf=|usr=}}{{26392224 }} gab.com Text Critical role of phospholipase A2 group IID in age-related susceptibility to severe acute respiratory syndrome-CoV infection JO: J Exp Med http://www.kidney.de/pget.php?&tw=1&pmid=26392224 #FOAvip Oxidative stress and chronic low-grade inflammation in the lungs are associated with aging and may contribute to age-related immune dysfunction. To maintain lung homeostasis, chronic inflammation is countered by enhanced expression of proresolving/antiinflammatory factors. Here, we show that age-dependent increases of one such factor in the lungs, a phospholipase A2 (PLA2) group IID (PLA2G2D) with antiinflammatory properties, contributed to worse outcomes in mice infected with severe acute respiratory syndrome-coronavirus (SARS-CoV). Strikingly, infection of mice lacking PLA2G2D expression (Pla2g2d(-/-) mice) converted a uniformly lethal infection to a nonlethal one (>80% survival), subsequent to development of enhanced respiratory DC migration to the draining lymph nodes, augmented antivirus T cell responses, and diminished lung damage. We also observed similar effects in influenza A virus-infected middle-aged Pla2g2d(-/-) mice. Furthermore, oxidative stress, probably via lipid peroxidation, was found to induce PLA2G2D expression in mice and in human monocyte-derived macrophages. Thus, our results suggest that directed inhibition of a single inducible phospholipase, PLA2G2D, in the lungs of older patients with severe respiratory infections is potentially an attractive therapeutic intervention to restore immune function. Twit Text FOAVip Critical role of phospholipase A2 group IID in age-related susceptibility to severe acute respiratory syndrome-CoV infection ????J Exp Med http://www.kidney.de/pget.php?&tw=1&pmid=26392224 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26392224 #FOAvip English Wikipedia <ref>{{Cite pmid|26392224 }}</ref> Critical role of phospholipase A2 group IID in age-related susceptibility to severe acute respiratory syndrome-CoV infection #MMPMID26392224 Vijay R ; Hua X ; Meyerholz DK ; Miki Y ; Yamamoto K ; Gelb M ; Murakami M ; Perlman S J Exp Med 2015[Oct]; 212 (11 ): 1851-68 PMID26392224 show ga Oxidative stress and chronic low-grade inflammation in the lungs are associated with aging and may contribute to age-related immune dysfunction. To maintain lung homeostasis, chronic inflammation is countered by enhanced expression of proresolving/antiinflammatory factors. Here, we show that age-dependent increases of one such factor in the lungs, a phospholipase A2 (PLA2) group IID (PLA2G2D) with antiinflammatory properties, contributed to worse outcomes in mice infected with severe acute respiratory syndrome-coronavirus (SARS-CoV). Strikingly, infection of mice lacking PLA2G2D expression (Pla2g2d(-/-) mice) converted a uniformly lethal infection to a nonlethal one (>80% survival), subsequent to development of enhanced respiratory DC migration to the draining lymph nodes, augmented antivirus T cell responses, and diminished lung damage. We also observed similar effects in influenza A virus-infected middle-aged Pla2g2d(-/-) mice. Furthermore, oxidative stress, probably via lipid peroxidation, was found to induce PLA2G2D expression in mice and in human monocyte-derived macrophages. Thus, our results suggest that directed inhibition of a single inducible phospholipase, PLA2G2D, in the lungs of older patients with severe respiratory infections is potentially an attractive therapeutic intervention to restore immune function. |*Disease Susceptibility [MESH] |Age Factors [MESH] |Animals [MESH] |CD11c Antigen/analysis [MESH] |Dendritic Cells/physiology [MESH] |Group II Phospholipases A2/*physiology [MESH] |Humans [MESH] |Immunity, Innate [MESH] |Lipids/analysis [MESH] |Lung/immunology [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Oxidative Stress [MESH]Critical role of phospholipase A2 group IID in age-related susceptibil(epmc).pdf DeepDyve Pubget Overpricing