Upregulation of Platelet-Activating Factor Receptor Expression and Lyso-Platelet-Activating Factor Isoforms in Human Nasal Polyp Tissues

Author:

Roca-Ferrer Jordi12,Pérez-González Maria12,Alobid Isam1234,Tubita Valeria124,Fuentes Mireya12,Bantulà Marina1,Muñoz-Cano Rosa145ORCID,Valero Antonio125ORCID,Izquierdo Iñaki6,Mullol Joaquim1234ORCID

Affiliation:

1. Clinical and Experimental Respiratory Immunoallergy (IRCE), Clinic Foundation for Biomedical Research-August Pi Sunyer Biomedical Research Institute (FRCB-IDIBAPS), 08036 Barcelona, Spain

2. CIBER of Respiratory Diseases (CIBERES), Health Institute Carlos III, 28029 Madrid, Spain

3. Rhinology Unit & Smell Clinic, ENT Department, Hospital Clínic Barcelona, 08036 Barcelona, Spain

4. Faculty of Medicine, Universitat de Barcelona, 08036 Barcelona, Spain

5. Allergy Department, Hospital Clínic, Universitat de Barcelona, 08036 Barcelona, Spain

6. Clinical Development & Medical Advise, R&D, NOUCOR, 08184 Palau Solità i Plegamans, Spain

Abstract

Background: The Platelet-Activating Factor (PAF)/receptor (PAFR) system is involved in asthma and allergic rhinitis; however, its role in chronic rhinosinusitis (CRS) is still unclear. This study aimed to assess the expression of PAFR and the concentration of Lyso-PAF isoforms in the nasal polyps (NP) of patients suffering from CRS with/without comorbidities such as asthma and NSAID-exacerbated respiratory disease (N-ERD) compared to healthy nasal mucosa (NM) from control subjects. Methods: NM (n = 8) and NP tissues were obtained from patients undergoing surgery for septal deviation/turbinate hypertrophy or endoscopic sinus surgery, respectively. Three phenotypes were studied: CRSwNP with no asthma (n = 6), CRSwNP with non-steroidal anti-inflammatory drug (NSAID)-tolerant asthma (n = 6), and CRSwNP with NSAID-exacerbated respiratory disease (n = 6). PAFR protein and mRNA were assessed via immunochemistry, immunofluorescence, Western blot, and real-time quantitative PCR. Lyso-PAF isoforms (C16, C18, and C18:1) were quantified via mass spectrometry. Results: PAFR protein was expressed in the NM and NP, concretely in epithelial cells and submucosal glands. Compared to NM, PAFR mRNA expression was higher in all NP phenotypes (p < 0.05) while all Lyso-PAF isoform concentrations were higher in the NP from asthmatic patients (p < 0.05). Lyso-PAF C16 and C18 concentrations were higher in the NP from asthmatic patients than in the NP from patients without asthma. Conclusions: The PAF/PAFR system could play a pathophysiological role in CRSwNP pathogenesis.

Funder

NOUCOR/Uriach Group

Publisher

MDPI AG

Subject

General Medicine

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