Ty -jour t1-流感病毒感染增加了人类小气道上皮细胞JF的ACE2表达和脱落 - 欧洲呼吸杂志S. au -crue，Taylor Au -Nall，Jordan M.Au -Foster，Daniel Au -Sajuthi，Satria Au -Correll -Correll，Kelly A. Au -Nakamura，Nakamura，Mari Au -Everman，Jamie L. Au -Jamie L. Au -Downey，Gregory P.Au -Seibold，Max A. Au -Bridges，James P. Au -Serban，Karina A. Au -Chu，Hong Wei Au -Petrache，Irina Y1-2021/07/01 UR- http：//www.qdcxjkg.com/content/58/1/2003988.Abstract N2-由严重急性急性呼吸综合征2（SARS-COV-2）引起的冠状病毒病2019（COVID-19）的背景患者表现出高呼吸病毒感染率的高率流感A（IAV），提示致病性相互作用。我们研究了IAV如何增加CoVID-19-19-lung疾病的风险，重点关注受体血管紧张素-CONVERTING酶（ACE）2和蛋白酶TMPRSS2，它们在SARS-COV-2的细胞内吸收中进行合作，我们发现，我们发现，使用远端人类非肺匀浆的单细胞RNA测序，在基线时，ACE2在ACE2下，在ACE2上最小表达。基础，杯状，纤毛和分泌的上皮细胞填充小气道。我们专注于人类小气道上皮细胞（SAEC），这是病毒感染后肺损伤发病机理的中心。来自非疾病的供体肺的原发性SAEC在顶端感染了IAV（在空气 - 液体界面上）具有IAV（最多3×105 pfu; 〜1多重感染）显着增强了ACE2的表达，与STAT1，A的表达相似，A STAT1，A，A转录因子被病毒激活。 IAV increased the apparent electrophoretic mobility of intracellular ACE2 and generated an ACE2 fragment (90 kDa) in apical secretions, suggesting cleavage of this receptor. In addition, IAV increased the expression of two proteases known to cleave ACE2, sheddase ADAM17 (TACE) and TMPRSS2 and increased the TMPRSS2 zymogen and its mature fragments, implicating proteolytic autoactivation.Conclusion These results indicate that IAV amplifies the expression of molecules necessary for SARS-CoV-2 infection of the distal lung. Furthermore, post-translational changes in ACE2 by IAV may increase vulnerability to lung injury such as acute respiratory distress syndrome during viral co-infections. These findings support efforts in the prevention and treatment of influenza infections during the COVID-19 pandemic.Influenza virus infection of cells lining the small airways increases the expression of molecules required for SARS-CoV-2 uptake in a manner that predicts increased severity of lung disease in those co-infected with influenza and coronaviruses https://bit.ly/3nu1WAo ER -