Original article
Published: 2025-05-06

impact of the bitter taste receptor on the predisposition to chronic rhinosinusitis

Department of Otolaryngology, Centre of Postgraduate Medical Education, Marymoncka 99/103, 01-813 Warsaw, Poland
https://orcid.org/0000-0003-4211-7664
Department of Experimental Immunotherapy, Maria Sklodowska-Curie Institute- Oncology Center, Roentgena 5, 02-781 Warsaw, Poland
https://orcid.org/0000-0001-7723-1198
Cardinal Stefan Wyszynski Univeristy in Warsaw
Department of Otolaryngology, Centre of Postgraduate Medical Education, Marymoncka 99/103, 01-813 Warsaw, Poland
https://orcid.org/0000-0003-1311-8377
Faculty of Medicine, Collegium Medicum, Cardinal Stefan Wyszynski University, Dewajtis 5, 01-815 Warsaw, Poland
https://orcid.org/0009-0006-7990-453X
Department of Experimental Immunotherapy, Maria Sklodowska-Curie Institute- Oncology Center, Roentgena 5, 02-781 Warsaw, Poland
https://orcid.org/0000-0002-0151-2417
Department of Experimental Immunotherapy, Maria Sklodowska-Curie Institute- Oncology Center, Roentgena 5, 02-781 Warsaw, Poland
https://orcid.org/0000-0001-7723-1198
genetics chronic rhinosinusitis CRS TAS2R38 bitter taste receptor

Abstract

Objectives: Genetic polymorphisms of bitter taste receptor 2 member 38 (TAS2R38), expressed in the cilia of sinonasal epithelial cells, have been proposed as contributors to chronic rhinosinusitis (CRS).

Methods: We assessed the impact of the genetically determined TAS2R38 structure on predisposition to CRS and correlated the expression of the TAS2R38 with haplotypes. 86 patients (60 CRS patients, 26 controls) undergoing nasal surgery were enrolled. PCR reactions to identify single nucleotide polymorphisms in genes encoding TAS2R38 were performed. TAS2R38 expression in the sinus mucosa tissues was assessed by immunohistochemistry.

Results: Among CRS patients, the protective genotype PAV/PAV of the TAS2R38 was observed with the lowest frequency. Immunohistochemistry displayed significant overexpression of TAS2R38 in CRS patients and among patients with non-functional AVI/AVI genotype. Under inflammatory conditions, the TAS2R38 was found to translocate from the cell membrane.

Conclusions: Genetically determined TAS2R38 polymorphism may influence susceptibility to CRS. The AVI haplotype seems to be an independent risk factor for CRS. Additionally, TAS2Rs and related signaling pathways might create a unique group of therapeutic targets in CRS.

Affiliations

Karolina Dżaman

Department of Otolaryngology, Centre of Postgraduate Medical Education, Marymoncka 99/103, 01-813 Warsaw, Poland

Elżbieta Sarnowska

Department of Experimental Immunotherapy, Maria Sklodowska-Curie Institute- Oncology Center, Roentgena 5, 02-781 Warsaw, Poland

Karolina Piskadlo-Zborowska

Cardinal Stefan Wyszynski Univeristy in Warsaw

Katarzyna Czerwaty

Department of Otolaryngology, Centre of Postgraduate Medical Education, Marymoncka 99/103, 01-813 Warsaw, Poland

Rafał Jowik

Faculty of Medicine, Collegium Medicum, Cardinal Stefan Wyszynski University, Dewajtis 5, 01-815 Warsaw, Poland

Małgorzata Stachowiak

Department of Experimental Immunotherapy, Maria Sklodowska-Curie Institute- Oncology Center, Roentgena 5, 02-781 Warsaw, Poland

Elżbieta Sarnowska

Department of Experimental Immunotherapy, Maria Sklodowska-Curie Institute- Oncology Center, Roentgena 5, 02-781 Warsaw, Poland

Copyright

© Società Italiana di Otorinolaringoiatria e chirurgia cervico facciale , 2025

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