Altered levels of IFN-γ, IL-4, and IL-5 depend on the
Humans
Pulmonary Disease, Chronic Obstructive
/ genetics
Polymorphism, Single Nucleotide
Male
Female
Toll-Like Receptor 4
/ genetics
Middle Aged
Interferon-gamma
/ genetics
Genotype
Aged
Interleukin-4
/ genetics
Biomass
Genetic Predisposition to Disease
Interleukin-5
/ genetics
Smoke
/ adverse effects
Mexico
Adult
Smokers
Smoking
/ adverse effects
COPD
SNPs
biomass-burning smoke
cytokines
tobacco smoke
Journal
Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960
Informations de publication
Date de publication:
2024
2024
Historique:
received:
02
04
2024
accepted:
10
07
2024
medline:
14
8
2024
pubmed:
14
8
2024
entrez:
14
8
2024
Statut:
epublish
Résumé
Chronic obstructive pulmonary disease (COPD) is associated with tobacco smoking and biomass-burning smoke exposure. Toll-like receptor 4 ( We enrolled 2,092 participants and divided them into two comparisons according to their environmental exposure. SNPs were genotyped using TaqMan probes. Serum cytokine levels (IL-4, IL-5, IL-6, IL-10, and INF-γ) were quantified by ELISA. The rs4986790 AA genotype in COPD-TS was associated with a higher COPD risk (OR = 3.53). Haplotype analysis confirmed this association, identifying a block containing the rs4986790 allele (A-C, OR = 3.11). COPD-TS exhibited elevated IL-6, IL-4, and IL-5 levels compared with smokers without COPD (SWOC), whereas COPD-BBS displayed higher IFN-γ, IL-6, and IL-10 levels. The AA carriers in the COPD-TS group had elevated IL-4, IL-5, and IFN-γ compared with carriers of AG or GG. The rs4986790 common allele and the A-C haplotype (rs4986790-rs4986791) were associated with a higher COPD risk in smokers; COPD patients carrying the AA genotype showed increased pro-inflammatory cytokines.
Identifiants
pubmed: 39139567
doi: 10.3389/fimmu.2024.1411408
pmc: PMC11319291
doi:
Substances chimiques
Toll-Like Receptor 4
0
Interferon-gamma
82115-62-6
TLR4 protein, human
0
Interleukin-4
207137-56-2
Interleukin-5
0
Smoke
0
IL4 protein, human
0
IL5 protein, human
0
IFNG protein, human
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1411408Informations de copyright
Copyright © 2024 Gutiérrez-Romero, Falfán-Valencia, Ramírez-Venegas, Hernández-Zenteno, Flores-Trujillo, Sansores-Martínez, Ramos-Martínez and Pérez-Rubio.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.