Th2 cytokine signaling through IL-4Rα increases eotaxin-3 secretion and tension in human esophageal smooth muscle

Author:

Nelson Melissa R.1,Zhang Xi1,Podgaetz Eitan2,Wang Xuan3,Zhang Qiuyang1ORCID,Pan Zui4ORCID,Spechler Stuart Jon1ORCID,Souza Rhonda F.1ORCID

Affiliation:

1. Department of Medicine, Center for Esophageal Diseases, Baylor University Medical Center and Center for Esophageal Research, Baylor Scott and White Research Institute, Dallas, Texas, United States

2. Center for Thoracic Surgery, Center for Esophageal Diseases, Baylor University Medical Center and Center for Esophageal Research, Baylor Scott and White Research Institute, Dallas, Texas, United States

3. Biostatistics Core, Baylor Scott and White Research Institute, Dallas, Texas, United States

4. College of Nursing and Health Innovation, The University of Texas at Arlington, Arlington, Texas, United States

Abstract

We have found that Th2 cytokines increase eotaxin-3 secretion and tension in esophageal smooth muscle (ESM) cells via IL-4Rα signaling. Unlike esophageal epithelial cells, ESM cells do not express H+-K+-ATPase, and omeprazole does not inhibit their cytokine-stimulated eotaxin-3 secretion or tension. An IL-4Rα blocking antibody reduces both eotaxin-3 secretion and tension induced by Th2 cytokines in ESM cells, suggesting that an agent such as dupilumab might be preferred for patients with EoE with esophageal muscle involvement.

Funder

Baylor Scott & White Research Institute

Publisher

American Physiological Society

Subject

Physiology (medical),Gastroenterology,Hepatology,Physiology

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