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Updated: Nov 23, 2025
Author Spotlight: Investigating the Pathophysiology of Eosinophilic Esophagitis
Published on: May 10, 2024
Type 2 Immunity and Age Modify Gene Expression of Coronavirus-induced Disease 2019 Receptors in Eosinophilic
Austin W T Chiang1,2, Loan D Duong3, Tetsuo Shoda4
1Department of Bioengineering.
Abstract:
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.
Insights
Type 2 immunity and pediatric age may protect against SARS-CoV-2 gastrointestinal infections. This is due to lower expression of angiotensin-converting enzyme-2 (ACE2) in the GI tract, a key entry point for the virus.
Area of Science:
- Immunology
- Gastroenterology
- Virology
Background:
- Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) can infect the gastrointestinal (GI) tract.
- SARS-CoV-2 entry into host cells relies on angiotensin-converting enzyme-2 (ACE2) and TMPRSS2.
- Eosinophilic gastrointestinal disorders (EGIDs) involve chronic type 2 (T2) inflammation.
Purpose of the Study:
- To investigate the impact of T2 inflammation on SARS-CoV-2 viral entry gene expression in the GI tract.
- To analyze ACE2 and TMPRSS2 gene expression in pediatric EGIDs and normal adult esophagi.
Main Methods:
- Utilized publicly available RNA-sequencing datasets.
- Compared gene expression of ACE2 and TMPRSS2 in pediatric eosinophilic esophagitis (EoE), eosinophilic gastritis (EG), and normal adult esophagi.
Main Results:
- No significant difference in ACE2/TMPRSS2 expression was found in EoE or EG compared to controls.
- ACE2 gene expression was significantly lower in esophagi from children (with or without EoE) and adults with EoE compared to normal adult esophagi.
Conclusions:
- Decreased ACE2 expression in the GI tract of children and adults with EoE suggests a potential protective effect against SARS-CoV-2 infection.
- Type 2 immunity and pediatric age may confer protection against SARS-CoV-2 GI infection due to reduced ACE2 expression.
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