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Asthma is a chronic respiratory condition for which new therapeutic avenues, including anti-inflammatory drugs like mast cell stabilizers and anti-IgE treatments, continue to be developed.
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Modulating endoplasmic reticulum stress attenuates mast cell degranulation.

Jialiang Fan1, Longpeng Ma1, Bailing Xie2

  • 1Department of Pediatric Otolaryngology, Shenzhen Hospital, and Third School of Clinical Medicine, Southern Medical University, Shenzhen, China; Guangdong Provincial Key Laboratory of Regional Immunity and Diseases, Shenzhen, China; Institute of Allergy & Immunology, Shenzhen University School of Medicine, State Key Laboratory of Respiratory Disease Shenzhen University Division, Shenzhen, China.

International Immunopharmacology
|December 6, 2023
PubMed
Summary

Endoplasmic reticulum (ER) stress drives mast cell degranulation and allergic symptoms. Inhibiting the X-box-1 binding protein (XBP1) pathway suppresses this degranulation, offering a potential therapeutic strategy for allergic rhinitis.

Keywords:
AirwayAllergyEndoplasmic reticulumMast cellMucosa

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Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Medicine

Background:

  • Mast cell degranulation is a key factor in allergic reactions.
  • Endoplasmic reticulum (ER) stress is implicated in allergic disease pathogenesis.
  • The precise mechanisms of mast cell degranulation require further elucidation.

Purpose of the Study:

  • To investigate the role of ER stress in mast cell degranulation.
  • To identify molecular pathways linking ER stress to mast cell mediator release.

Main Methods:

  • Utilized bone marrow-derived and airway-isolated mast cells.
  • Assessed the impact of ER stress modulation on mast cell mediator release.
  • Employed RNA sequencing (RNAseq) to analyze mast cell gene expression.

Main Results:

  • Mast cell sensitization was found to increase ER stress.
  • X-box-1 binding protein (XBP1) activity correlated with mast cell degranulation.
  • Modulating ER stress or XBP1 influenced mast cell mediator release.
  • XBP1 activation of spleen tyrosine kinase (Syk) promoted mediator release.
  • Semaphorin 3A inhibited mast cell mediator release, mitigating experimental allergic rhinitis (AR).

Conclusions:

  • ER stress is significantly associated with mast cell degranulation.
  • Inhibiting XBP1, a key ER stress molecule, effectively suppresses mast cell degranulation.
  • Targeting the ER stress pathway, specifically XBP1, presents a viable strategy for managing allergic rhinitis.