Association of +67 G/A and -426 T/C Polymorphism in Eotaxin (CCL11) Gene with Psoriasis Phenotypes
Jazyk angličtina Země Švýcarsko Médium electronic
Typ dokumentu časopisecké články
PubMed
40149440
PubMed Central
PMC11941883
DOI
10.3390/genes16030288
PII: genes16030288
Knihovny.cz E-zdroje
- Klíčová slova
- CCL11, polymorphism, psoriasis,
- MeSH
- alely MeSH
- chemokin CCL11 * genetika MeSH
- dospělí MeSH
- fenotyp MeSH
- genetická predispozice k nemoci MeSH
- genetické asociační studie MeSH
- genotyp MeSH
- jednonukleotidový polymorfismus * MeSH
- lidé středního věku MeSH
- lidé MeSH
- psoriáza * genetika patologie MeSH
- senioři MeSH
- studie případů a kontrol MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- CCL11 protein, human MeSH Prohlížeč
- chemokin CCL11 * MeSH
Background/Objectives: Several gene targets were identified for psoriasis. Some are currently being explored as potential therapeutic targets, including CCL11. Our task was to prove a possible association of single-nucleotide polymorphisms +67 G/A and -426 T/C in the eotaxin gene (CCL11, 17q 21.3) with the development and clinical aspects of psoriasis as an immune-based dermatological disease and evaluate its relationship to potential comorbidities. Material and Methods: In total, 460 patients with psoriasis were included in the case-control and genotype-phenotype study together with 167 control persons of similar age and sex distributions without a personal and/or family history of chronic disease of the skin. Two eotaxin gene polymorphisms were detected from isolated DNA via standard PCR, restriction analysis methods, and horizontal electrophoresis. Results: No significant case-control differences in the frequency of the CCL11 genotype in both polymorphisms were observed. In polymorphism +67 G/A, a significant increase in the AA genotype in patients with psoriasis guttata compared to plaque psoriasis was found (p = 0.006). A significant association of the A allele in psoriatic patients with a personal history of allergy was found (p = 0.02). The A alle was also significantly associated with a family history of psoriasis (p = 0.00008). In men, a higher risk of a delayed start of psoriasis (later than 40 years) associated with the T allele of -426 T/C polymorphism (p = 0.0007) was found. When double genotypes of both polymorphisms were evaluated, we observed significant differences in double genotype distribution between men with and without a family history of allergy (Pdg = 0.0005) and between those with and without affected siblings (Pdg = 0.03). In women with psoriasis, a higher risk of the TT genotype of -426 T/C polymorphism in patients with a personal history of diabetes (p = 0.001) as well as in patients with both a personal history of cardiovascular disease and diabetes (p = 0.00005) was proved. When double genotypes of both polymorphisms were evaluated, the significance of double genotype difference between those with and without personal history of diabetes was very high (Pdg = 0.0002). Similarly, the significance of the double genotype difference between those with and without personal history of cardiovascular diseases and diabetes was very high (Pdg = 0.000001). Conclusions: CCL11 is considered one of the basic chemokines responsible for the origin and development of immune-based reactions. Based on our results, we suggest that the +67 G/A CCL11 polymorphism should be considered as a gene modulator of psoriasis in specific subgroups of patients.
Department of Pathophysiology Faculty of Medicine Masaryk University 625 00 Brno Czech Republic
Psychiatrie Brno Martinkova 253 7 Černá Pole 612 00 Brno Czech Republic
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