期刊
CELL RESEARCH
卷 30, 期 12, 页码 1078-1087出版社
SPRINGERNATURE
DOI: 10.1038/s41422-020-00435-z
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资金
- National Natural Science Foundation of China [81788101, 81530080, 81773062, 91942314]
- Chinese Academy of Medical Sciences (CAMS) Initiative for Innovative Medicine ((CAMS-I2M)) [2020-I2M-CoV19-007, 2020-I2M-CoV19-003, 2016-I2M-1-007, 2017-I2M-006]
Silent hypoxia has emerged as a unique feature of coronavirus disease 2019 (COVID-19). In this study, we show that mucins are accumulated in the bronchoalveolar lavage fluid (BALF) of COVID-19 patients and are upregulated in the lungs of severe respiratory syndrome coronavirus 2 (SARS-CoV-2)-infected mice and macaques. We find that induction of either interferon (IFN)-beta or IFN-gamma upon SARS-CoV-2 infection results in activation of aryl hydrocarbon receptor (AhR) signaling through an IDO-Kyn-dependent pathway, leading to transcriptional upregulation of the expression of mucins, both the secreted and membrane-bound, in alveolar epithelial cells. Consequently, accumulated alveolar mucus affects the blood-gas barrier, thus inducing hypoxia and diminishing lung capacity, which can be reversed by blocking AhR activity. These findings potentially explain the silent hypoxia formation in COVID-19 patients, and suggest a possible intervention strategy by targeting the AhR pathway.
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