Small intestine cells at risk for COVID-19 infection in IBD patients
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High expression of ACE2 and TMPRSS2 in the small intestines may support gastrointestinal-correlated replication of SARS-COV-2, according to a study published in Gastroenterology.
“We investigated two aspects of COVID-19 biology and describe one of the most detailed protein and gene expression characterizations of COVID-19 receptors in the intestinal tract to date,” Saurabh Mehandru, MD, principal investigator, and associate professor of gastroenterology, Icahn School of Medicine at Mount Sinai, said in a Mount Sinai press release. “We have found that the SARS-CoV-2 receptor, ACE2, is abundantly expressed by the lining of the small intestines, implying that small intestinal cells have the potential to get infected by COVID-19.”
High expression of ACE2 and TMPRSS2 in the small intestines may support gastrointestinal-correlated replication of SARS-COV-2
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Mehandru and colleagues used large cohorts of patients with IBD including the Mount Sinai Crohn’s and Colitis Registry, the GSE57945 series, GSE100833 series and GSE73661 series to study the intersections between COVID-19, intestinal inflammation and IBD treatment.
Results showed expression of ACE2 on the small bowel enterocyte brush border, which supports the intestinal infectivity by SARS-CoV-2. Investigators noted ACE2 and TMPRSS2 receptor expression in the uninflamed intestines was not affected by biologic or non-biologic IBD medications.
According to researchers, age and sex and not smoking modulated ACE2; however, age and sex did not modulate TMPRSS2 mRNA expression in the IBD colon.
“Importantly, this intersecting biology appeared to be enriched in genes that change upon anti-IBD medication use in IBD patients, suggesting that some of the IBD medications could be used to treat COVID-19,” co-leading author, Carmen Argmann, MD, associate professor, genetics and genomic sciences, Icahn School of Medicine at Mount Sinai, said in the press release. “This study reminds us of the value of investigating COVID-19 not only as a ‘new’ disease but also how it might relate to ‘old/common’ diseases for which a rich mechanistic and therapeutic knowledge base already exists and can be rapidly re-contextualized.”
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