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  3. Interaction between airway basal cells, mast cells and type 2 immunity contributes to epithelial barrier dysfunction in allergic rhinitis

Interaction between airway basal cells, mast cells and type 2 immunity contributes to epithelial barrier dysfunction in allergic rhinitis

  • Mucosal Immunol. 2026 Feb 21:S1933-0219(26)00021-8. doi: 10.1016/j.mucimm.2026.02.004.
Emma Ruysseveldt 1,  Tine Wils 2,  Daan Rodiers 2,  Toon Ieven 3,  Janne Goossens 2,  Ellen Dilissen 2,  Jonathan Cremer 2,  Dominique M A Bullens 4,  Katleen Martens 2,  Brecht Steelant 2,  Peter W Hellings 5
Affiliations

Affiliations

  • 1 KU Leuven, Department of Microbiology, Immunology and Transplantation, Allergy and Clinical Immunology Research Group, Leuven, Belgium. Electronic address: [email protected].
  • 2 KU Leuven, Department of Microbiology, Immunology and Transplantation, Allergy and Clinical Immunology Research Group, Leuven, Belgium.
  • 3 KU Leuven, Department of Microbiology, Immunology and Transplantation, Allergy and Clinical Immunology Research Group, Leuven, Belgium; University Hospitals Leuven, Department of General Internal Medicine, Division of Allergy and Clinical Immunology, Belgium.
  • 4 KU Leuven, Department of Microbiology, Immunology and Transplantation, Allergy and Clinical Immunology Research Group, Leuven, Belgium; University Hospitals Leuven, Clinical Department of Paediatrics, Leuven, Belgium.
  • 5 KU Leuven, Department of Microbiology, Immunology and Transplantation, Allergy and Clinical Immunology Research Group, Leuven, Belgium; University Hospitals Leuven, Clinical Department of Otorhinolaryngology, Head and Neck Surgery, Leuven, Belgium; Upper Airways Research Laboratory, UGhent, Ghent 9000, Belgium. Electronic address: [email protected].
PMID: 41730474 DOI: 10.1016/j.mucimm.2026.02.004
Abstract

Basal cell dysfunction contributes to the pathophysiology of chronic inflammatory airway disorders and is linked to persistent epithelial barrier defects. Epithelial integrity dysfunction, basal cell hyperplasia and metaplasia have been described in allergic rhinitis (AR). However, it remains unclear how basal cell progenitor functions are regulated and if basal cells contribute to type 2 inflammatory responses. Here, we report on the proinflammatory and sensory role of basal cells in AR. Using primary nasal basal cells from controls and AR patients, we demonstrate that Der p1 induces basal cell cytokine (IL-6) and chemokine (CXCL1, CXCL6, CXCL8, SCF) expression and/or release via PAR2, suggesting a role for basal cells as environmental sensors and inflammatory regulators. Using nasal biopsies, we show that mast cells are attracted to the epithelium in AR, likely via basal cell-derived SCF, and induce basal cell chemokine (CCL26, CXCL1, CXCL6, SCF) release via histamine and tryptase in vitro. Finally, histamine, IL-4 and IL-13 impair primary nasal basal cell proliferation, mobility, barrier formation, and differentiation in in vitro cellular assays, illustrating basal cell dysfunction in AR.

Keywords

Allergic rhinitis; Basal cells; Chronic barrier dysfunction; Mast cells; Upper airway inflammation.

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