Type 2 Immunity and Age Modify Gene Expression of Coronavirus-induced Disease 2019 Receptors in Eosinophilic Gastrointestinal Disorders.
Journal
Journal of pediatric gastroenterology and nutrition
ISSN: 1536-4801
Titre abrégé: J Pediatr Gastroenterol Nutr
Pays: United States
ID NLM: 8211545
Informations de publication
Date de publication:
01 05 2021
01 05 2021
Historique:
pubmed:
5
1
2021
medline:
22
6
2021
entrez:
4
1
2021
Statut:
ppublish
Résumé
Infection with severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) can lead to coronavirus-induced disease 2019 (COVID-19). The gastrointestinal (GI) tract is now an appreciated portal of infection. SARS-CoV-2 enters host cells via angiotensin-converting enzyme-2 (ACE2) and the serine protease TMPRSS2. Eosinophilic gastrointestinal disorders (EGIDs) are inflammatory conditions caused by chronic type 2 (T2) inflammation. the effects of the T2 atopic inflammatory milieu on SARS-COV-2 viral entry gene expression in the GI tract is poorly understood. We analyzed tissue ACE2 and TMPRSS2 gene expression in pediatric eosinophilic esophagitis (EoE), eosinophilic gastritis (EG), and in normal adult esophagi using publicly available RNA-sequencing datasets. Similar to findings evaluating the airway, there was no difference in tissue ACE2/TMPRSS2 expression in EoE or EG when compared with control non-EoE/EG esophagus/stomach. ACE2 gene expression was significantly lower in esophagi from children with or without EoE and from adults with EoE as compared with normal adult esophagi. Type 2 immunity and pediatric age could be protective for infection by SARS-CoV-2 in the gastrointestinal tract because of decreased expression of ACE2.
Identifiants
pubmed: 33394891
doi: 10.1097/MPG.0000000000003032
pii: 00005176-202105000-00019
pmc: PMC8048378
doi:
Substances chimiques
Peptidyl-Dipeptidase A
EC 3.4.15.1
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
718-722Subventions
Organisme : NCATS NIH HHS
ID : U2C TR002818
Pays : United States
Organisme : NIDDK NIH HHS
ID : R03 DK118310
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK078392
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI092135
Pays : United States
Organisme : NIAID NIH HHS
ID : K24 AI135034
Pays : United States
Organisme : NIAID NIH HHS
ID : U54 AI117804
Pays : United States
Organisme : NIGMS NIH HHS
ID : R35 GM119850
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK124266
Pays : United States
Informations de copyright
Copyright © 2020 by European Society for Pediatric Gastroenterology, Hepatology, and Nutrition and North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition.
Déclaration de conflit d'intérêts
T.S. has received research support from JSPS Overseas Research Fellowships and is a co-inventor of patents owned by Cincinnati Children's Hospital Medical Center. M.E.R. is a consultant for Pulm One, Spoon Guru, ClostraBio, Serpin Pharm, Celgene, Astra Zeneca, Allakos, Arena Pharmaceuticals, GlaxoSmith Kline, Guidepoint and Suvretta Capital Management, and has an equity interest in the first 4 listed, and royalties from reslizumab (Teva Pharmaceuticals), PEESSv2 (Mapi Research Trust) and UpToDate. M.E.R. is an inventor of patents owned by Cincinnati Children's Hospital. S.S.A. is a co-inventor of oral viscous budesonide patented by UCSD and licensed by Takeda, has royalties from UpToDate and is a consultant for Aimmune, Astra Zeneca, Astellas, and Gossamer. The other authors claim no conflict of interest.
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