Coding variants of TLR2 and TLR4 genes do not substantially contribute to prosthetic joint infection
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Inflammation Research
ORIGINAL RESEARCH PAPER
Coding variants of TLR2 and TLR4 genes do not substantially contribute to prosthetic joint infection Frantisek Mrazek • Jiri Gallo • Anna Stahelova Martin Petrek
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Received: 26 September 2012 / Accepted: 29 January 2013 / Published online: 17 February 2013 Ó Springer Basel 2013
Abstract 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.
Responsible Editor: Andras Falus. F. Mrazek (&) A. Stahelova M. Petrek Laboratory of Immunogenomics and Immunoproteomics, Department of Immunology, Faculty of Medicine and Dentistry, Palacky University, I. P. Pavlova str. 6, 775 20 Olomouc, Czech Republic e-mail: [email protected] J. Gallo Department of Orthopaedics, Faculty of Medicine and Dentistry, Palacky University and University Hospital, I. P. Pavlova 6, 775 20 Olomouc, Czech Republic
Conclusion Our data suggest that structural genetic variants of the receptors TLR2 and TLR4 do not substantially affect the risk of prosthetic joint infection. Keywords Total joint prosthesis Gene polymorphism Genetic risk Susceptibility Total joint arthroplasty
Introduction Total joint arthroplasty (TJA) is a very effective medical procedure that substantially improves quality of life in patients with end-stage joint affections. Despite careful management and pre/intra/postoperative preventative measures, TJA is complicated by prosthetic joint infection (PJI) in up to 2.5 % of patients, dependent on anatomical localization of the arthroplasty [1, 2]. Bacteria cause the vast majority of PJI; of them, the most frequent causative agents are Staphylococci [3]. PJI usually requires revision surgery and, apart from detrimental effects on patients, multiplies the overall cost of TJA in affected individuals [4]. Several ‘‘conventional’’ risk factors contributing to PJI have been identified in epidemiological studies such as diabetes mellitus, rheumatoid arthritis, higher individual risk scores for anaesthesia, revision arthroplasty, and wound complications including superficial infections [5, 6]. Recently, the role of heritable factors in indiv
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