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Eosinophilic esophagitis drives tissue fibroblast regenerative programs toward pathologic dysfunction.

Medet Jumabay1, Edsel M Abud2, Kevin Okamoto1

  • 1Department of Pediatrics, University of California, San Diego, Calif; Division of Allergy Immunology, University of California, San Diego, Calif.

The Journal of Allergy and Clinical Immunology
|December 1, 2024
PubMed
Summary
This summary is machine-generated.

Chronic inflammation in eosinophilic esophagitis (EoE) creates pathogenic fibroblasts that hinder tissue repair. Targeting adenosine triphosphate handling and CD73 may restore fibroblast function and improve healing in type 2 inflammatory diseases.

Keywords:
ATPCD73Eosinophilic esophagitisadenosinefibrosisremodeling

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Area of Science:

  • Gastroenterology
  • Immunology
  • Cell Biology

Background:

  • Pathologic tissue remodeling, scarring, and rigidity are hallmarks of inflammatory, autoimmune, and allergic diseases.
  • Eosinophilic esophagitis (EoE) involves tissue remodeling, leading to dysphagia and esophageal strictures, yet underlying molecular mechanisms are unclear.
  • Fibroblast dysfunction is implicated in EoE-associated tissue remodeling.

Purpose of the Study:

  • To investigate the hypothesis that chronic EoE inflammation induces pathogenic fibroblasts with impaired tissue regeneration and motility.
  • To elucidate the molecular mechanisms driving fibroblast dysfunction in EoE.

Main Methods:

  • Single-cell RNA sequencing to analyze transcriptional profiles of EoE and healthy fibroblasts.
  • Fluorescence-activated cell sorting (FACS) and functional assays to assess fibroblast differentiation, migration, and CD73 activity.
  • In vivo and in vitro experiments to induce and rescue EoE fibroblast dysfunctions.

Main Results:

  • EoE fibroblasts exhibit proinflammatory and pro-rigidity transcriptional programs, retaining chondrocyte-like differentiation but losing adipocyte-like capacity.
  • EoE fibroblasts show increased migration and decreased CD73 expression and activity, indicating aberrant extracellular adenosine triphosphate handling.
  • EoE fibroblast dysfunction can be recapitulated in healthy fibroblasts by reducing CD73 activity and reversed by adenosine repletion.

Conclusions:

  • Chronic EoE inflammation drives pathogenic fibroblast phenotypes characterized by altered tissue regeneration and motility.
  • Perturbed extracellular adenosine triphosphate handling and CD73 activity are key mechanisms in EoE fibroblast dysfunction.
  • Modulating adenosine triphosphate handling and CD73 offers a potential therapeutic strategy for improving tissue regeneration in EoE and other type 2 inflammatory diseases.