@article{c50494d41ea64ffbbc5e2b2f3a72fcc0,
title = "Expression of SARS-CoV-2 entry molecules ACE2 and TMPRSS2 in the gut of patients with IBD",
abstract = "Background: Patients with inflammatory bowel disease (IBD) have intestinal inflammation and are treated with immune-modulating medications. In the face of the coronavirus disease-19 pandemic, we do not know whether patients with IBD will be more susceptible to infection or disease. We hypothesized that the viral entry molecules angiotensin I converting enzyme 2 (ACE2) and transmembrane serine protease 2 (TMPRSS2) are expressed in the intestine. We further hypothesized that their expression could be affected by inflammation or medication usage. Methods: We examined the expression of Ace2 and Tmprss2 by quantitative polymerase chain reacion in animal models of IBD. Publicly available data from organoids and mucosal biopsies from patients with IBD were examined for expression of ACE2 and TMPRSS2. We conducted RNA sequencing for CD11b-enriched cells and peripheral and lamina propria T-cells from well-annotated patient samples. Results: ACE2 and TMPRSS2 were abundantly expressed in the ileum and colon and had high expression in intestinal epithelial cells. In animal models, inflammation led to downregulation of epithelial Ace2. Expression of ACE2 and TMPRSS2 was not increased in samples from patients with compared with those of control patients. In CD11b-enriched cells but not T-cells, the level of expression of ACE2 and TMPRSS2 in the mucosa was comparable to other functional mucosal genes and was not affected by inflammation. Anti-tumor necrosis factor drugs, vedolizumab, ustekinumab, and steroids were linked to significantly lower expression of ACE2 in CD11b-enriched cells. Conclusions: The viral entry molecules ACE2 and TMPRSS2 are expressed in the ileum and colon. Patients with IBD do not have higher expression during inflammation; medical therapy is associated with lower levels of ACE2. These data provide reassurance for patients with IBD.",
keywords = "Coronavirus, Crohn disease, Ulcerative colitis",
author = "Burgueno, {Juan F.} and Adrian Reich and Hajar Hazime and Quintero, {Maria A.} and Irina Fernandez and Julia Fritsch and Santander, {Ana M.} and Nivis Brito and Damas, {Oriana M.} and Amar Deshpande and Kerman, {David H.} and Lanyu Zhang and Zhen Gao and Yuguang Ban and Lily Wang and Judith Pignac-Kobinger and Abreu, {Maria T.}",
note = "Funding Information: From the *Division of Gastroenterology, Department of Medicine, University of Miami Miller School of Medicine, Miami, Florida, USA; †Center for Computational Biology and Bioinformatics, The Scripps Research Institute-Florida, Jupiter, Florida, USA; ‡Biostatistics and Bioinformatics Shared Resource, Sylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, Miami, Florida, USA Supported by: This work was supported by grants from the National Institute of Diabetes and Digestive and Kidney Diseases (grant number R01DK09907), Takeda Pharmaceutical, U.S.A. (grant number IISR-2014-1000892), Inc., Pfizer (ASPIRE award number WI227247), The Micky & Madeleine Arison Family Foundation Crohn{\textquoteright}s & Colitis Discovery Laboratory, and the Martin Kalser Chair (to coauthor MTA). Funding Information: Conflicts of interest: AR has served as a consultant to GenapSys Inc. AD has served as a scientific advisory board member for GI Health Foundation, has a funded grant from Takeda, and received honoraria from AMBIM. DHK has served as a scientific advisory board member for AbbVie and as a consultant for Cleveland Clinic and currently serves as a trainer or lecturer for PRIME Continuing Medical Education and The Academy for Continued Healthcare Learning. MTA has served as a scientific advisory board member for Boehringer Ingelheim Pharmaceuticals, Gilead, AbbVie, Seres Therapeutics, Shire, and Landos Biopharma; serves as a trainer or lecturer for Imedex, Focus Medical Communications, and Cornerstones Health, Inc.; has served as a consultant for Ferring Pharmaceuticals, Allergan, Amgen, Celltrion Healthcare CO, Millennium Pharmaceuticals, Theravance Biopharma Inc., and UCB Biopharma SRL; and has funded projects by Pfizer, Prometheus Laboratories, and Takeda Pharmaceuticals. OMD received honoraria from Pfizer and has a funded grant from Pfizer. This does not alter the authors{\textquoteright} adherence to the journal{\textquoteright}s policies on sharing data and materials. All other authors declare no conflict of interest.",
year = "2020",
month = jun,
day = "1",
doi = "10.1093/ibd/izaa085",
language = "English (US)",
volume = "26",
pages = "797--808",
journal = "Inflammatory Bowel Diseases",
issn = "1078-0998",
publisher = "John Wiley and Sons Inc.",
number = "6",
}