Coding variants of TLR2 and TLR4 genes do not substantially contribute to prosthetic joint infection
Jazyk angličtina Země Švýcarsko Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
- MeSH
- artroplastika MeSH
- infekce spojené s protézou genetika MeSH
- infekce MeSH
- jednonukleotidový polymorfismus MeSH
- klouby chirurgie MeSH
- lidé středního věku MeSH
- lidé MeSH
- protézy a implantáty škodlivé účinky MeSH
- senioři MeSH
- stafylokokové infekce genetika MeSH
- Staphylococcus MeSH
- toll-like receptor 2 genetika MeSH
- toll-like receptor 4 genetika MeSH
- Check Tag
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- TLR2 protein, human MeSH Prohlížeč
- TLR4 protein, human MeSH Prohlížeč
- toll-like receptor 2 MeSH
- toll-like receptor 4 MeSH
OBJECTIVE AND DESIGN: Prosthetic joint infection (PJI) is a severe complication of total joint arthroplasty (TJA). We conducted a genetic association study that investigated whether selected coding variants of the genes for Toll-like receptors (TLR)2 and TLR4 may contribute to genetic susceptibility for PJI. SUBJECTS AND METHODS: In total, 350 patients with TJA (98 with PJI/252 without PJI), and 189 unrelated healthy Czech individuals without TJA were enrolled in our study. Three missense polymorphisms of the genes encoding for TLR2 (TLR2 R753Q, rs5743708) and TLR4 (TLR4 D299G, rs4986790 and T399I, rs4986791) were genotyped by "TaqMan" assay. RESULTS: The frequencies of less common variants for the investigated TLR2/TLR4 polymorphisms in healthy individuals were similar to those observed in other Caucasian populations. Importantly, the distribution of TLR2/TLR4 genotype alleles did not differ between the patients with PJI and the control groups of patients with nonseptic prostheses/healthy individuals. CONCLUSION: Our data suggest that structural genetic variants of the receptors TLR2 and TLR4 do not substantially affect the risk of prosthetic joint infection.
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J Infect. 2010 Dec;61(6):443-8 PubMed
Am J Hypertens. 2002 Feb;15(2 Pt 1):201-5 PubMed
J Immunol. 2011 Jun 1;186(11):6585-96 PubMed
Ann Rheum Dis. 2007 Aug;66(8):1116-20 PubMed
Nucleic Acids Res. 1988 Feb 11;16(3):1215 PubMed
Inflamm Res. 2012 Mar;61(3):177-88 PubMed
J Innate Immun. 2009;1(4):350-7 PubMed
Clin Chem Lab Med. 2011 Sep;49(9):1427-37 PubMed
N Engl J Med. 2011 Jan 6;364(1):60-70 PubMed
Otolaryngol Head Neck Surg. 2011 Jan;144(1):96-100 PubMed
J Bone Joint Surg Am. 2009 Jan;91(1):38-47 PubMed
ANZ J Surg. 2011 Jan;81(1-2):32-9 PubMed
Orthop Traumatol Surg Res. 2010 Apr;96(2):124-32 PubMed
J Arthroplasty. 2007 Feb;22(2):265-70 PubMed
BMC Immunol. 2012 May 08;13:25 PubMed
Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub. 2012 Sep;156(3):248-52 PubMed
J Hepatol. 2012 May;56(5):1207-1208 PubMed
Hum Immunol. 2011 Jan;72(1):47-53 PubMed
Immunity. 2011 May 27;34(5):637-50 PubMed
PLoS One. 2010 Aug 10;5(8):e12087 PubMed
Acta Orthop. 2010 Oct;81(5):542-7 PubMed
Mediators Inflamm. 2010;2010:781235 PubMed
New Microbiol. 2008 Jan;31(1):97-104 PubMed