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UC San Diego
Interleukin 9 Alters Epithelial Barrier and E-cadherin in Eosinophilic Esophagitis.
- Author(s): Doshi, Ashmi
- Khamishon, Rebecca
- Rawson, Renee
- Duong, Loan
- Dohil, Lucas
- Myers, Stephen J
- Bell, Braxton
- Dohil, Ranjan
- Newbury, Robert O
- Barrett, Kim E
- Kurten, Richard C
- Aceves, Seema S
- et al.
Published Web Locationhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6344288/
No data is associated with this publication.
BackgroundEosinophilic esophagitis (EoE) is a chronic TH2-assocated inflammatory condition accompanied by substantial impairments in epithelial barrier function and increased numbers of interleukin 9 (IL-9) expressing inflammatory cells. While IL-9 is known to affect barrier function in the intestine, the functional effects of IL-9 on the esophagus are unclear. Herein we aimed to understand the expression of the IL-9 receptor and effects of IL-9 on the epithelium in EoE.
MethodsWe used esophageal biopsies from pediatric EoE patients with active and inactive disease to analyze the expression of the IL-9 receptor, the adherens junction protein E-cadherin and the tight junction protein claudin-1. We treated primary human esophageal epithelial cells with IL-9 to understand its effects on E-cadherin expression and function.
ResultsActive EoE subjects had increased epithelial expression of IL-9 receptor mRNA and protein (P < 0.05) and decreased membrane bound E-cadherin (P < 0.01) and claudin-1 (P < 0.05) expression. IL-9 receptor expression and mislocalized claudin-1 positively correlated and while membrane bound E-cadherin expression negatively correlated with the degree of histologic epithelial remodeling (P < 0.05). IL-9 decreased epithelial resistance in stratified primary human esophageal epithelial cells (P < 0.01) and membrane bound E-cadherin in epithelial cell monolayers (P < 0.01).
ConclusionsThese data suggest that IL-9, its receptor, and its effects on E-cadherin may be important mechanisms for epithelial barrier disruption in EoE.
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