| Literature DB >> 26433033 |
Kornélia Szabó1, Hilda Polyánka2, Ágnes Kiricsi3, Mónika Révész4, Ida Vóna5, Zsolt Szabó6, Zsolt Bella3, Edit Kadocsa3, Lajos Kemény7, Márta Széll8, Andor Hirschberg9.
Abstract
Inflammation plays a central role in the pathogenesis of chronic rhinosinusitis (CRS), and TNFα is a key pro-inflammatory cytokine in the pathogenesis of this disease. In our previous studies, we showed that the TNFA -308A allele is a genetic predisposition factor in a subgroup of aspirin-sensitive (ASA+) CRS patients suffering from nasal polyps (NP) in the Hungarian population. To determine whether the TNF -308A allele or the presence of a complex, extended ancestral haplotype (8.1AH) located on chromosome 6 is responsible for the previously observed genetic effect, we performed a case-control study for examining the frequency of 8.1AH carriers in controls and in subgroups of CRS patients. Our novel observations demonstrate that the presence of the 8.1AH may be responsible for the development of severe forms of CRS (CRSwNP, ASA+) and strengthen the clinical observation that CRS patients can be classified into clinically and genetically different subgroups.Entities:
Keywords: 8.1 ancestral haplotype (8.1AH); Chronic rhinosinusitis (CRS); Nasal polyp (NP); Single nucleotide polymorphism (SNP)
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Year: 2015 PMID: 26433033 DOI: 10.1016/j.humimm.2015.09.048
Source DB: PubMed Journal: Hum Immunol ISSN: 0198-8859 Impact factor: 2.850