Variation in the IL1B, TNF and IL6 genes and individual susceptibility to prosthetic joint infection
Jazyk angličtina Země Anglie, Velká Británie Médium electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
22568934
PubMed Central
PMC3475038
DOI
10.1186/1471-2172-13-25
PII: 1471-2172-13-25
Knihovny.cz E-zdroje
- MeSH
- artroplastika * MeSH
- dospělí MeSH
- genetická predispozice k nemoci * MeSH
- genetické asociační studie MeSH
- infekce spojené s protézou genetika MeSH
- interleukin-1beta genetika MeSH
- interleukin-6 genetika MeSH
- lidé MeSH
- mladý dospělý MeSH
- mutační analýza DNA MeSH
- polymorfismus genetický MeSH
- protézy kloubů škodlivé účinky MeSH
- studie případů a kontrol MeSH
- TNF-alfa genetika MeSH
- Check Tag
- dospělí MeSH
- lidé MeSH
- mladý dospělý MeSH
- mužské pohlaví MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- interleukin-1beta MeSH
- interleukin-6 MeSH
- TNF-alfa MeSH
BACKGROUND: Prosthetic joint infection (PJI) is an important failure mechanism of total joint arthroplasty (TJA). Here we examine whether the particular genetic variants can lead to increased susceptibility to PJI development. RESULTS: We conducted a genetic-association study to determine whether PJI could be associated with functional cytokine gene polymorphisms (CGP) influencing on innate immunity response. A case-control design was utilized and previously published criteria for PJI were included to distinguish between cases and control subjects with/without TJA. Six single nucleotide polymorphisms (SNPs) located in the genes for interleukin-1beta (SNP: IL1B-511, +3962), tumour necrosis factor alpha (TNF-308, -238) and interleukin-6 (IL6-174, nt565) were genotyped in 303 Caucasian (Czech) patients with TJA (89 with PJI / 214 without PJI), and 168 unrelated healthy Czech individuals without TJA. The results showed that carriers of the less common IL1B-511*T allele were overrepresented in the group of TJA patients with PJI (69%) in comparison with those that did not develop PJI (51%, p = 0.006, p(corr) = 0.037) and with healthy controls (55%, p = 0.04, p(corr) = N.S.). There was no significant difference in the distribution of the remaining five investigated CGPs and their haplotypes between groups. CONCLUSION: A functional variant of the gene encoding for IL-1beta was preliminarily nominated as a genetic factor contributing to the susceptibility to PJI. Our results should be independently replicated; studies on the functional relevance of IL1B gene variants in PJI are also needed.
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