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Estrogen receptor-α signaling increases allergen-induced IL-33 release and airway inflammation. | LitMetric

AI Article Synopsis

  • Group 2 innate lymphoid cells (ILC2) are influenced by IL-33, which leads to increased production of inflammatory cytokines IL-5 and IL-13, contributing to airway inflammation, particularly in response to allergens.
  • The study investigates the role of estrogen receptors, specifically ER-α and ER-β, in regulating ILC2 interactions and the release of IL-33 during allergen challenges in female mice.
  • Findings indicate that estrogen receptor-α signaling enhances IL-33 release, elevates ILC2 cytokine production and airway inflammation, while tamoxifen treatment reduces these inflammatory responses.

Article Abstract

Background: Group 2 innate lymphoid cells (ILC2) are stimulated by IL-33 to increase IL-5 and IL-13 production and airway inflammation. While sex hormones regulate airway inflammation, it remained unclear whether estrogen signaling through estrogen receptor-α (ER-α, Esr1) or ER-β (Esr2) increased ILC2-mediated airway inflammation. We hypothesize that estrogen signaling increases allergen-induced IL-33 release, ILC2 cytokine production, and airway inflammation.

Methods: Female Esr1 , Esr2 , wild-type (WT), and IL33 eGFP mice were challenged with Alternaria extract (Alt Ext) or vehicle for 4 days. In select experiments, mice were administered tamoxifen or vehicle pellets for 21 days prior to challenge. Lung ILC2, IL-5 and IL-13 production, and BAL inflammatory cells were measured on day 5 of Alt Ext challenge model. Bone marrow from WT and Esr1 female mice was transferred (1:1 ratio) into WT female recipients for 6 weeks followed by Alt Ext challenge. hBE33 cells and normal human bronchial epithelial cells (NHBE) were pretreated with 17β-estradiol (E2), propyl-pyrazole-triol (PPT, ER-α agonist), or diarylpropionitrile (DPN, ER-β agonist) before allergen challenge to determine IL-33 gene expression and release, extracellular ATP release, DUOX-1 production, and necrosis.

Results: Alt Ext challenged Esr1 , but not Esr2 , mice had decreased IL-5 and IL-13 production, BAL eosinophils, and IL-33 release compared to WT mice. Tamoxifen decreased IL-5 and IL-13 production and BAL eosinophils. IL-33eGFP + epithelial cells were decreased in Alt Ext challenged Esr1 mice compared to WT mice. 17β-E2 or PPT, but not DPN, increased IL-33 gene expression, release, and DUOX-1 production in hBE33 or NHBE cells.

Conclusion: Estrogen receptor -α signaling increased IL-33 release and ILC2-mediated airway inflammation.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7790897PMC
http://dx.doi.org/10.1111/all.14491DOI Listing

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