CD73+ Epithelial Progenitor Cells That Contribute to Homeostasis and Renewal Are Depleted in Eosinophilic Esophagitis

Takeo Hara(Children's Hospital of Philadelphia), Yuta Kasagi(Children's Hospital of Philadelphia), Joshua Wang(Children's Hospital of Philadelphia), Masaru Sasaki(Children's Hospital of Philadelphia), Bailey Aaron(Children's Hospital of Philadelphia), Adam Karami(Temple University), Masataka Shimonosono(Columbia University Irving Medical Center), Rieko Shimonosono(Columbia University Irving Medical Center), Hisatsugu Maekawa(Columbia University Irving Medical Center), Lauren Dolinsky(Children's Hospital of Philadelphia), Benjamin J. Wilkins(Children's Hospital of Philadelphia), Jeremy Klein(Children's Hospital of Philadelphia), Jane Wei(Children's Hospital of Philadelphia), Kathryn L. Nunes(Children's Hospital of Philadelphia), Kristle L. Lynch(University of Pennsylvania), Jonathan M. Spergel(Children's Hospital of Philadelphia), Kathryn E. Hamilton(Children's Hospital of Philadelphia), Melanie A. Ruffner(Children's Hospital of Philadelphia), Tatiana A. Karakasheva(Children's Hospital of Philadelphia), Kelly A. Whelan(Temple University), Hiroshi Nakagawa(Columbia University Irving Medical Center), Amanda B. Muir(Children's Hospital of Philadelphia)
Cellular and Molecular Gastroenterology and Hepatology
January 1, 2022
Cited by 48Open Access
Full Text

Abstract

BACKGROUND & AIMS: cells within the basal population of human esophageal epithelium and clarified the biological significance of these cells in the EoE epithelium. METHODS: populations and seeded these groups in organoid culture to evaluate the organoid formation rate and organoid size. We used RNA interference to knock down CD73 in esophageal organoids to evaluate organoid formation rates and size. We evaluated the effects of signal transducer and activator of transcription 6 (STAT6) signaling inhibition by RNA interference, a STAT6 inhibitor, AS1517499, as well as the proton pump inhibitor omeprazole. RESULTS: population. CONCLUSIONS: self-renewal population by helper T cell 2 cytokines in EoE milieu may be perpetuating epithelial injury. Future therapies targeting epithelial restitution in EoE could decrease the need for immune modulation and steroid therapy.


Related Papers

No related papers found

Powered by citation graph analysis