Quantitative Proteomic Analysis of the Expression of SARS-CoV-2 Receptors in the Gut of Patients with Chronic Enterocolitis
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The cellular entry of severe respiratory syndrome coronavirus-2 (SARS-CoV-2) is mediated by interaction with the human angiotensin-converting enzyme 2 (ACE2), a receptor that is expressed on both lung and intestinal epithelial cells. We performed a quantitative proteomic analysis to investigate the expression of possible receptors for SARS-CoV-2 in the intestinal mucosa of 23 patients with chronic colitis. ACE2 expression was low and remained unaltered in the gut of patients with ulcerative colitis (UC), Crohn’s disease (CD), intestinal Behćet’s disease (BD), and intestinal tuberculosis (TB), when compared with that of healthy individuals. Additionally, the expression levels of some probable co-receptors, including dipeptidyl peptidase 4 (DPP4), aminopeptidase N (AMPN), and glutamyl aminopeptidase (AMPE), were unchanged in the affected UC, CD, intestinal BD, and intestinal TB colon mucosa samples. In conclusion, gut inflammation associated with chronic colitis does not mediate a further increase in the cellular entry of SARS-CoV-2.
Abstract
The cellular entry of severe respiratory syndrome coronavirus-2 (SARS-CoV-2) is mediated by interaction with the human angiotensin-converting enzyme 2 (ACE2), a receptor that is expressed on both lung and intestinal epithelial cells. We performed a quantitative proteomic analysis to investigate the expression of possible receptors for SARS-CoV-2 in the intestinal mucosa of 23 patients with chronic colitis. ACE2 expression was low and remained unaltered in the gut of patients with ulcerative colitis (UC), Crohn’s disease (CD), intestinal Behćet’s disease (BD), and intestinal tuberculosis (TB), when compared with that of healthy individuals. Additionally, the expression levels of some probable co-receptors, including dipeptidyl peptidase 4 (DPP4), aminopeptidase N (AMPN), and glutamyl aminopeptidase (AMPE), were unchanged in the affected UC, CD, intestinal BD, and intestinal TB colon mucosa samples. In conclusion, gut inflammation associated with chronic colitis does not mediate a further increase in the cellular entry of SARS-CoV-2.
참고문헌 (12)
- Guan WJ, "Clinical characteristics of coronavirus disease 2019 in China", N Engl J Med, 382, pp.1708~1720 (2020)
- Hoffmann M, "SARS-CoV-2 cell entry depends on ACE2 and TMPRSS2 and is blocked by a clinically proven protease inhibitor", Cell, 181, pp.271~280 (2020)
- Harmer D, "Quantitative mRNA expression profiling of ACE 2, a novel homologue of angiotensin converting enzyme", FEBS Lett, 532, pp.107~110 (2002)
- Goyal P, "Clinical characteristics of COVID-19 in New York City", N Engl J Med, 382, pp.2372~2374 (2020)
- Xiao F, "Evidence for gastrointestinal infection of SARS-CoV-2", Gastroenterology, 158, pp.1831~1833 (2020)
- Qi F, "Single cell RNA sequencing of 13human tissues identify cell types and receptors of human coronaviruses", Biochem Biophys Res Commun, 526, pp.135~140 (2020)
- Garg M, "Imbalance of the renin-angiotensin system may contribute to inflammation and fibrosis in IBD : a novel therapeutic target", Gut, 69, pp.841~851 (2020)
- Ning L, "Quantitative proteomic analysis reveals the deregulation of nicotinamide adenine dinucleotide metabolism and CD38 in inflammatory bowel disease", Biomed Res Int, 2019, pp.3950628~ (2019)
- Chang Kyun Lee, "A new opportunity for innovative inflammatory bowel disease research: the moderate-to-severe ulcerative colitis in Korea (MOSAIK) cohort study", Intestinal research, 17(1), pp.1~5 (2019), 대한장연구학회[DOI]
- An P, "Prevention of COVID-19 in patients with inflammatory bowel disease in Wuhan, China", Lancet Gastroenterol Hepatol, 5, pp.525~527 (2020)
- Imai Y, "Angiotensinconverting enzyme 2 protects from severe acute lung failure", Nature, 436, pp.112~116 (2005)
- Patel AB, "Nasal ACE2 Levels and COVID-19 in Children", JAMA, 323, pp.2386~2387 (2020)