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10.1152/ajplung.00345.2020 http://scihub22266oqcxt.onion/10.1152/ajplung.00345.2020 32878480!7516381!32878480     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=32878480&cmd=llinks): Failed to open stream: HTTP request failed! 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Elevated FiO(2) increases SARS-CoV-2 co-receptor expression in respiratory tract epithelium |pdf=|usr=}}{{32878480}} gab.com Text Elevated FiO(2) increases SARS-CoV-2 co-receptor expression in respiratory tract epithelium JO: Am J Physiol Lung Cell Mol Physiol http://www.kidney.de/pget.php?&tw=1&pmid=32878480 #FOAvip The severity of coronavirus disease 2019 (COVID-19) is linked to an increasing number of risk factors, including exogenous (environmental) stimuli such as air pollution, nicotine, and cigarette smoke. These three factors increase the expression of angiotensin I converting enzyme 2 (ACE2), a key receptor involved in the entry of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-the etiological agent of COVID-19-into respiratory tract epithelial cells. Patients with severe COVID-19 are managed with oxygen support, as are at-risk individuals with chronic lung disease. To date, no study has examined whether an increased fraction of inspired oxygen (FiO(2)) may affect the expression of SARS-CoV-2 entry receptors and co-receptors, including ACE2 and the transmembrane serine proteases TMPRSS1, TMPRSS2, and TMPRSS11D. To address this, steady-state mRNA levels for genes encoding these SARS-CoV-2 receptors were assessed in the lungs of mouse pups chronically exposed to elevated FiO(2), and in the lungs of preterm-born human infants chronically managed with an elevated FiO(2). These two scenarios served as models of chronic elevated FiO(2) exposure. Additionally, SARS-CoV-2 receptor expression was assessed in primary human nasal, tracheal, esophageal, bronchial, and alveolar epithelial cells, as well as primary mouse alveolar type II cells exposed to elevated oxygen concentrations. While gene expression of ACE2 was unaffected, gene and protein expression of TMPRSS11D was consistently upregulated by exposure to an elevated FiO(2). These data highlight the need for further studies that examine the relative contribution of the various viral co-receptors on the infection cycle, and point to oxygen supplementation as a potential risk factor for COVID-19. Twit Text FOAVip Elevated FiO(2) increases SARS-CoV-2 co-receptor expression in respiratory tract epithelium ????Am J Physiol Lung Cell Mol Physiol http://www.kidney.de/pget.php?&tw=1&pmid=32878480 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32878480 #FOAvip English Wikipedia <ref>{{Cite pmid|32878480}}</ref> Elevated FiO(2) increases SARS-CoV-2 co-receptor expression in respiratory tract epithelium #MMPMID32878480 Myti D; Gunjak M; Casado F; Khaghani Raziabad S; Nardiello C; Vadasz I; Herold S; Pryhuber G; Seeger W; Morty RE Am J Physiol Lung Cell Mol Physiol 2020[Oct]; 319 (4): L670-L674 PMID32878480show ga The severity of coronavirus disease 2019 (COVID-19) is linked to an increasing number of risk factors, including exogenous (environmental) stimuli such as air pollution, nicotine, and cigarette smoke. These three factors increase the expression of angiotensin I converting enzyme 2 (ACE2), a key receptor involved in the entry of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-the etiological agent of COVID-19-into respiratory tract epithelial cells. Patients with severe COVID-19 are managed with oxygen support, as are at-risk individuals with chronic lung disease. To date, no study has examined whether an increased fraction of inspired oxygen (FiO(2)) may affect the expression of SARS-CoV-2 entry receptors and co-receptors, including ACE2 and the transmembrane serine proteases TMPRSS1, TMPRSS2, and TMPRSS11D. To address this, steady-state mRNA levels for genes encoding these SARS-CoV-2 receptors were assessed in the lungs of mouse pups chronically exposed to elevated FiO(2), and in the lungs of preterm-born human infants chronically managed with an elevated FiO(2). These two scenarios served as models of chronic elevated FiO(2) exposure. Additionally, SARS-CoV-2 receptor expression was assessed in primary human nasal, tracheal, esophageal, bronchial, and alveolar epithelial cells, as well as primary mouse alveolar type II cells exposed to elevated oxygen concentrations. While gene expression of ACE2 was unaffected, gene and protein expression of TMPRSS11D was consistently upregulated by exposure to an elevated FiO(2). These data highlight the need for further studies that examine the relative contribution of the various viral co-receptors on the infection cycle, and point to oxygen supplementation as a potential risk factor for COVID-19. |Alveolar Epithelial Cells/metabolism[MESH] |Angiotensin-Converting Enzyme 2[MESH] |Animals[MESH] |Betacoronavirus[MESH] |COVID-19[MESH] |Cells, Cultured[MESH] |Coronavirus Infections/*pathology[MESH] |Female[MESH] |Humans[MESH] |Male[MESH] |Membrane Proteins/genetics/*metabolism[MESH] |Mice[MESH] |Mice, Inbred C57BL[MESH] |Oxygen/administration & dosage/analysis[MESH] |Pandemics[MESH] |Peptidyl-Dipeptidase A/*metabolism[MESH] |Pneumonia, Viral/*pathology[MESH] |Receptors, Virus/metabolism[MESH] |Respiratory Mucosa/*metabolism[MESH] |Risk Factors[MESH] |SARS-CoV-2[MESH] |Serine Endopeptidases/genetics/*metabolism[MESH] |Serine Proteases/genetics/*metabolism[MESH]Elevated FiO(2) increases SARS-CoV-2 co-receptor expression in respira(epmc).pdf DeepDyve Pubget Overpricing