共感染
细菌粘附素
微生物学
神经氨酸酶
生物
病毒学
纤维连接蛋白
甲型流感病毒
病毒
免疫学
毒力
细胞
基因
生物化学
遗传学
作者
Ning Li,Aihui Ren,Xiaoshuang Wang,Xin Fan,Yong Zhao,George F. Gao,P. Patrick Cleary,Beinan Wang
标识
DOI:10.1073/pnas.1414422112
摘要
Significance Pneumonia caused by bacterial coinfection with influenza virus is the leading cause of mortality in influenza pandemics. TGF-β is known to be activated by influenza virus. In this study we demonstrated that cellular adhesins for bacteria, such as fibronectin and α5 integrin, are up-regulated in influenza viral infection. Inhibition of TGF-β impeded the up-regulation of these cellular adhesins and also influenza viral-enhanced bacterial adherence. In addition, we found that influenza viral-promoted bacterial adherence was dependent on bacterial fibronectin-binding protein. The results indicate that up-regulated expression of cellular adhesins by TGF-β, which is activated in influenza viral infection, increases host susceptibility to bacterial coinfection and suggest that TGF-β and host adhesion molecules are potential pharmaceutical targets for prevention of coinfection.
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