Abstract
BackgroundFor allergic disorders, the increasing prevalence over the past decade has been attributed in part to the lack of microbial burden in developed countries ('hygiene hypothesis'). Variation in genes encoding toll-like receptors (TLRs) as the receptor system for the first innate immune response to microbial stimuli has been implicated in various inflammatory diseases. We evaluated here the role of a coding variation, Ser249Pro, in the TLR6 gene in the pathogenesis of asthma, atopic dermatitis (AD) and chronic obstructive pulmonary disease (COPD).MethodsGenotyping of the Ser249Pro polymorphism in 68 unrelated adult patients and 132 unrelated children with asthma, 185 unrelated patients with COPD, 295 unrelated individuals with AD and 212 healthy control subjects was performed by restriction enzyme digestion.ResultsWe found a weak association of the 249Ser allele with childhood asthma (p = 0.03). Yet, significance was lost after Bonferroni correction. No association was evident for AD or COPD.ConclusionVariation in TLR6 might play a role in the pathogenesis of childhood asthma.
Highlights
For allergic disorders, the increasing prevalence over the past decade has been attributed in part to the lack of microbial burden in developed countries ('hygiene hypothesis')
The receptor system that constitutes the first, innate immune response to microbial stimuli consists of the family of toll-like receptors (TLRs), highly conserved receptor complexes that recognize pathogen-associated molecular patterns (PAMPs) [8]
Since the nucleotide substitution from C to T at position 744 in the TLR6 gene results in the creation of a new restriction site, the Ser249Pro polymorphism was genotyped by restriction enzyme digestion
Summary
The increasing prevalence over the past decade has been attributed in part to the lack of microbial burden in developed countries ('hygiene hypothesis'). We evaluated here the role of a coding variation, Ser249Pro, in the TLR6 gene in the pathogenesis of asthma, atopic dermatitis (AD) and chronic obstructive pulmonary disease (COPD). 10 different TLRs are known each of which recognizes a different spectrum of PAMPs. As activators of cytokine production in response to infections, TLRs are believed to be involved in the establishment of T helper (Th) immune responses in early life, counter-balancing the Th2-dominated cytokine spectrum at birth [9]. As activators of cytokine production in response to infections, TLRs are believed to be involved in the establishment of T helper (Th) immune responses in early life, counter-balancing the Th2-dominated cytokine spectrum at birth [9] Genetic variation in these receptors could influence susceptibility for both Th1- (e.g., autoimmune) and Th2mediated (e.g., allergic) diseases [9]
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