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10.1093/infdis/jit031 http://scihub22266oqcxt.onion/10.1093/infdis/jit031 23325916!ä!23325916 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=23325916&cmd=llinks): Failed to open stream: HTTP request failed! 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Leptin mediates the pathogenesis of severe 2009 pandemic influenza A(H1N1) infection associated with cytokine dysregulation in mice with diet-induced obesity |pdf=|usr=}}{{23325916}} gab.com Text Leptin mediates the pathogenesis of severe 2009 pandemic influenza A(H1N1) infection associated with cytokine dysregulation in mice with diet-induced obesity JO: J Infect Dis http://www.kidney.de/pget.php?&tw=1&pmid=23325916 #FOAvip BACKGROUND: Obesity is associated with a high circulating leptin level and severe 2009 pandemic influenza A virus subtype H1N1 (A[H1N1]pdm09) infection. The mechanism for severe lung injury in obese patients and the specific treatment strategy remain elusive. METHOD: We studied the pathogenesis of A(H1N1)pdm09 infection in a mouse model of diet-induced obesity. RESULTS: Obese mice had significantly higher initial pulmonary viral titer and mortality after challenge with A(H1N1)pdm09, compared with age-matched lean mice. Compared with lean mice, obese mice had heightened proinflammatory cytokine and chemokine levels and more severe pulmonary inflammatory damage. Furthermore, obese mice had a higher preexisting serum leptin level but a lower preexisting adiponectin level. Recombinant mouse leptin increased the interleukin 6 (IL-6) messenger RNA expression in mouse single-lung-cell preparations, mouse macrophages, and mouse lung epithelial cell lines infected with A(H1N1)pdm09. Administration of anti-leptin antibody improved the survival of infected obese mice, with associated reductions in pulmonary levels of the proinflammatory cytokines IL-6 and interleukin 1beta but not the pulmonary viral titer. CONCLUSIONS: Our findings suggest that preexisting high levels of circulating leptin contribute to the development of severe lung injury by A(H1N1)pdm09 in mice with diet-induced obesity. The therapeutic strategy of leptin neutralization for the reduction of proinflammatory responses and pulmonary damage in obese patients warrants further investigations. Twit Text FOAVip Leptin mediates the pathogenesis of severe 2009 pandemic influenza A(H1N1) infection associated with cytokine dysregulation in mice with diet-induced obesity ????J Infect Dis http://www.kidney.de/pget.php?&tw=1&pmid=23325916 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23325916 #FOAvip English Wikipedia <ref>{{Cite pmid|23325916}}</ref> Leptin mediates the pathogenesis of severe 2009 pandemic influenza A(H1N1) infection associated with cytokine dysregulation in mice with diet-induced obesity #MMPMID23325916 Zhang AJ; To KK; Li C; Lau CC; Poon VK; Chan CC; Zheng BJ; Hung IF; Lam KS; Xu A; Yuen KY J Infect Dis 2013[Apr]; 207 (8): 1270-80 PMID23325916show ga BACKGROUND: Obesity is associated with a high circulating leptin level and severe 2009 pandemic influenza A virus subtype H1N1 (A[H1N1]pdm09) infection. The mechanism for severe lung injury in obese patients and the specific treatment strategy remain elusive. METHOD: We studied the pathogenesis of A(H1N1)pdm09 infection in a mouse model of diet-induced obesity. RESULTS: Obese mice had significantly higher initial pulmonary viral titer and mortality after challenge with A(H1N1)pdm09, compared with age-matched lean mice. Compared with lean mice, obese mice had heightened proinflammatory cytokine and chemokine levels and more severe pulmonary inflammatory damage. Furthermore, obese mice had a higher preexisting serum leptin level but a lower preexisting adiponectin level. Recombinant mouse leptin increased the interleukin 6 (IL-6) messenger RNA expression in mouse single-lung-cell preparations, mouse macrophages, and mouse lung epithelial cell lines infected with A(H1N1)pdm09. Administration of anti-leptin antibody improved the survival of infected obese mice, with associated reductions in pulmonary levels of the proinflammatory cytokines IL-6 and interleukin 1beta but not the pulmonary viral titer. CONCLUSIONS: Our findings suggest that preexisting high levels of circulating leptin contribute to the development of severe lung injury by A(H1N1)pdm09 in mice with diet-induced obesity. The therapeutic strategy of leptin neutralization for the reduction of proinflammatory responses and pulmonary damage in obese patients warrants further investigations. |Animals[MESH] |Antibodies/administration & dosage/immunology[MESH] |Diet, High-Fat/adverse effects[MESH] |Disease Models, Animal[MESH] |Epithelium/immunology/pathology[MESH] |Female[MESH] |Influenza A Virus, H1N1 Subtype/*pathogenicity[MESH] |Interleukin-1beta/immunology[MESH] |Interleukin-6/genetics/*immunology[MESH] |Kaplan-Meier Estimate[MESH] |Leptin/*immunology/metabolism/pharmacology[MESH] |Lung/immunology/pathology/virology[MESH] |Macrophages/drug effects/immunology/virology[MESH] |Mice[MESH] |Mice, Inbred C57BL[MESH] |Mice, Obese[MESH] |Obesity/*immunology/virology[MESH] |Orthomyxoviridae Infections/immunology/*pathology/virology[MESH] |Pandemics[MESH] |Pneumonia/immunology/pathology/virology[MESH] |RNA, Messenger/analysis/genetics[MESH] |Recombinant Proteins/immunology/pharmacology[MESH]Leptin mediates the pathogenesis of severe 2009 pandemic influenza A(H(epmc).pdf DeepDyve Pubget Overpricing