TY  - JOUR
AB  - PURPOSE: Non-steroidal anti-inflammatory drug-exacerbated respiratory disease (N-ERD) is a phenotype of bronchial asthma that is characterized by a severe course and the presence of chronic rhinosinusitis (CRS) with nasal polyps. MicroRNAs (miRNAs) belong to a family of small, non-coding RNAs whose primary function is to regulate gene transcription. The aim of this study was to determine the miRNA profile and to validate selected miRNAs in biological material from the upper respiratory tract collected with a minimally-invasive method in patients with N-ERD. METHODS: The miRNA profile was assessed in subjects with N-ERD, CRS, and allergic asthma (AA), as well as healthy controls (HCs), using microarray technique. Following this, 6 miRNAs were validated using reverse transcription polymerase chain reaction in 77 subjects. RESULTS: The profiling identified 23 miRNAs whose expression significantly differed between patients with N-ERD and HCs. Based on these results, 6 miRNAs were selected for further validation. It was found that patients with N-ERD had significantly different expressions of miR-34a-5p and miR-22-5p compared to those with AA. In the whole study group, significant correlations were found between miR-7d-3p/miR-34a-5p/miR-22-5p and the presence of blood eosinophilia (r = 0.25, r = 0.28 and r = 0.26, for all P < 0.05). Forced expiratory volume in 1 second/forced vital capacity was correlated with miR-149a-5p expression (r = 0.27, P < 0.05). CONCLUSIONS: The results indicate that the miRNA profile in nasal mucosal lining fluid of patients with N-ERD differs from patients with AA, CRS, and compared to HCs. Some of the miRNAs selected on the basis of profiling may be involved in the regulation of eosinophilic inflammation in the respiratory tract. Our findings suggest that specific miRNAs may be considered as potential biomarkers of N-ERD.
AU  - Gajewski, A.*
AU  - Bekier, A.*
AU  - Frachowicz-Guereirro, K.*
AU  - Drożdż, I.*
AU  - Ćwikliński, R.*
AU  - Kurowski, M.*
AU  - Kowalski, M.L.*
AU  - Baumann, R.*
AU  - Schmidt-Weber, C.B.
AU  - Chaker, A.
AU  - Chałubiński, M.*
AU  - Wardzyńska, A.*
C1  - 74044
C2  - 57307
CY  - Rm 1705, Kumho Bldg 327-2, Changsindong, Jongno-gu, Seoul 110-540, South Korea
SP  - 226-240
TI  - Analysis of miRNA expression in patients with NSAID-exacerbated respiratory disease.
JO  - Allergy Asthma Immunol. Res.
VL  - 17
IS  - 2
PB  - Korean Acad Asthma Allergy & Clinical Immunology
PY  - 2025
SN  - 2092-7355
ER  - 

TY  - JOUR
AB  - PURPOSE: Numerous genes have been associated with allergic diseases (asthma, allergic rhinitis, and eczema), but they explain only part of their heritability. This is partly because most previous studies ignored complex mechanisms such as gene-environment (G-E) interactions and complex phenotypes such as co-morbidity. However, it was recently evidenced that the co-morbidity of asthma-plus-eczema appears as a sub-entity depending on specific genetic factors. Besides, evidence also suggest that gene-by-early life environmental tobacco smoke (ETS) exposure interactions play a role in asthma, but were never investigated for asthma-plus-eczema. To identify genetic variants interacting with ETS exposure that influence asthma-plus-eczema susceptibility. METHODS: To conduct a genome-wide interaction study (GWIS) of asthma-plus-eczema according to ETS exposure, we applied a 2-stage strategy with a first selection of single nucleotide polymorphisms (SNPs) from genome-wide association meta-analysis to be tested at a second stage by interaction meta-analysis. All meta-analyses were conducted across 4 studies including a total of 5,516 European-ancestry individuals, of whom 1,164 had both asthma and eczema. RESULTS: Two SNPs showed significant interactions with ETS exposure. They were located in 2 genes, NRXN1 (2p16) and TNS1 (2q35), never reported associated and/or interacting with ETS exposure for asthma, eczema or more generally for allergic diseases. TNS1 is a promising candidate gene because of its link to lung and skin diseases with possible interactive effect with tobacco smoke exposure. CONCLUSIONS: This first GWIS of asthma-plus-eczema with ETS exposure underlines the importance of studying sub-phenotypes such as co-morbidities as well as G-E interactions to detect new susceptibility genes.
AU  - Margaritte-Jeannin, P.*
AU  - Vernet, R.*
AU  - Budu-Aggrey, A.*
AU  - Ege, M.J.
AU  - Madore, A.M.*
AU  - Linhard, C.*
AU  - Mohamdi, H.*
AU  - von Mutius, E.
AU  - Granell, R.*
AU  - Demenais, F.*
AU  - Laprise, C.*
AU  - Bouzigon, E.*
AU  - Dizier, M.H.*
C1  - 68747
C2  - 54957
CY  - Rm 1705, Kumho Bldg 327-2, Changsindong, Jongno-gu, Seoul 110-540, South Korea
SP  - 779-794
TI  - TNS1 and NRXN1 genes interacting with early-life smoking exposure in asthma-plus-eczema susceptibility.
JO  - Allergy Asthma Immunol. Res.
VL  - 15
IS  - 6
PB  - Korean Acad Asthma Allergy & Clinical Immunology
PY  - 2023
SN  - 2092-7355
ER  -