Journal
PLOS ONE
Volume 16, Issue 3, Pages -Publisher
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0248730
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Funding
- NIH [NIDDK K08 DK111941]
- NCI Cancer Center Support Grant [P30 CA015704]
- Fred Hutchinson Cancer Research Center (Pathogen-Associated Malignancies Integrated Research Center, Microbiome Research Initiative)
- Washington Research Foundation
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Patients with gastrointestinal symptoms of COVID-19 tend to have worse prognosis. The gene Ace2, expressed in the gut and encoding the host protein targeted by SARS-CoV-2, may play a role in mitigating COVID-19 severity. Research suggests that the microbiome could potentially modulate Ace2 expression, impacting COVID-19 infection risk and disease severity.
COVID-19 (coronavirus disease 2019) patients exhibiting gastrointestinal symptoms are reported to have worse prognosis. Ace2 (angiotensin-converting enzyme 2), the gene encoding the host protein to which SARS-CoV-2 spike proteins bind, is expressed in the gut and therefore may be a target for preventing or reducing severity of COVID-19. Here we test the hypothesis that Ace2 expression in the gastrointestinal and respiratory tracts is modulated by the microbiome. We used quantitative PCR to profile Ace2 expression in germ-free mice, conventional raised specific pathogen-free mice, and gnotobiotic mice colonized with different microbiota. Intestinal Ace2 expression levels were significantly higher in germ-free mice compared to conventional mice. A similar trend was observed in the respiratory tract. Intriguingly, microbiota depletion via antibiotics partially recapitulated the germ-free phenotype, suggesting potential for microbiome-mediated regulation of Ace2 expression. Variability in intestinal Ace2 expression was observed in gnotobiotic mice colonized with different microbiota, partially attributable to differences in microbiome-encoded proteases and peptidases. Together, these data suggest that the microbiome may be one modifiable factor determining COVID-19 infection risk and disease severity.
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