BACKGROUND: Chronic rhinosinusitis (CRS) is believed to reflect an inflammatory response of the sinonasal mucosa to bacteria and/or fungi. Staphylococcus aureus, a gram-positive organism, is frequently implicated. Toll-like receptor 2 (TLR2) is involved in innate immunity, recognizing gram-positive organisms via detection of bacterial lipopeptides. As a poor response to sinus surgery has been associated with reduced levels of TLR2 expression, and given the frequent recovery of S. aureus in this condition, we suspected that polymorphisms in TLR2 genes are implicated in this condition. OBJECTIVE: To investigate the association between single nucleotide polymorphisms (SNPs) in the TLR2 gene and CRS. METHODS: Two hundred six patients with severe CRS and 200 controls were recruited prospectively. A maximally informative set of SNPs in the gene encoding TLR2 were selected from the HapMap data set and genotyped. RESULTS: Eleven of 12 SNPs were successfully genotyped. No significant associations could be detected for the SNPs tested within the limitations of our study, which has the power to detect only those SNPs with a relative risk of 2.0 or greater. CONCLUSIONS: Our findings do not support a role for polymorphisms in the TLR2 gene in the pathogenesis of CRS. Nevertheless, other genetic variants within genes regulating innate immunity may be involved and will require further assessment.
BACKGROUND:Chronic rhinosinusitis (CRS) is believed to reflect an inflammatory response of the sinonasal mucosa to bacteria and/or fungi. Staphylococcus aureus, a gram-positive organism, is frequently implicated. Toll-like receptor 2 (TLR2) is involved in innate immunity, recognizing gram-positive organisms via detection of bacterial lipopeptides. As a poor response to sinus surgery has been associated with reduced levels of TLR2 expression, and given the frequent recovery of S. aureus in this condition, we suspected that polymorphisms in TLR2 genes are implicated in this condition. OBJECTIVE: To investigate the association between single nucleotide polymorphisms (SNPs) in the TLR2 gene and CRS. METHODS: Two hundred six patients with severe CRS and 200 controls were recruited prospectively. A maximally informative set of SNPs in the gene encoding TLR2 were selected from the HapMap data set and genotyped. RESULTS: Eleven of 12 SNPs were successfully genotyped. No significant associations could be detected for the SNPs tested within the limitations of our study, which has the power to detect only those SNPs with a relative risk of 2.0 or greater. CONCLUSIONS: Our findings do not support a role for polymorphisms in the TLR2 gene in the pathogenesis of CRS. Nevertheless, other genetic variants within genes regulating innate immunity may be involved and will require further assessment.