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Loss of these beneficial microbes could reduce Treg abundance, tilting the immune system toward a pro-inflammatory phenotype [66]

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doi: 10.1128/mBio.01682-18 24 BrockmanK

Conclusion Based on these investigations with a model of normal small airway epithelia and other normal lung epithelial cells, we predict that increased TNF/NFB- and ENaC- dependent inflammation in the COVID-19 airway is due to inhibition of CFTR signaling by SARS-CoV-2 spike protein, thus inducing a pro-inflammatory clinical phenotype in lung epithelia