Abstract:

Aim: Specifically, endotoxin has raised important insight into the immune response and atopic diseases. It is possible that the immune dysregulation behind asthma (and endotoxin exposure) mostly occurs at the genetic level. Overall, it appears that a genetic predisposition to asthma exists and that fundamental mechanisms of the innate immune system may be involved. Polymorphisms of TLRs (Toll like receptors) and CD14 have been associated with response to endotoxin. Genetic variations may influence known effects or may create new associations. TLRs and endotoxin exposure and its association with asthma and allergies are controversial. Materials and Methods: This study comprised 165 cases from Ege University Medical Faculty, Paediatric Allergy and Pulmonology Polyclinic, the control group was formed from 117 healthy children and adolescents not thought to have any atopic illness. Total blood and eosinophil counts, Ig, G, M, A, values, total and spIgE values were recorded from the children of both groups and those in the patient group were given a skin prick test after having had spIgE values taken. Arg753Gln heterozygote, Gln753Gln homozygote, TLR2753 polymorphisms, Asp299Gly heterozygote, Gly299Gly homozygote, TLR4299 polymorphisms, Thr399Ile heterozygote, Ile399Ile homozygote and TLR4399 polymorphisms were researched in all cases. Polymorphisms for the TLRs were detected by polymerase chain reaction. Results: When evaluated from the angle of criteria such as atopic conditions in the family, household pets or attending a creche while under 6 months old, for each 3 genotypes there was no statistically significant difference between the cases showing a normal genotype and those showing polymorphism. In both the study and the control group no statistically significant difference was found between the genotype and normal distribution for each of the 3 genotypes (TLR2 75- p=0.9; TLR4 299 -p=0.65; TLR4 399 -p=0.72). Conclusion: Our study results showed no relationship between the development of allergic rhinitis and asthma and the genetic variants of the signalling pathway of the endotoxin receptors TLR2 and TLR4.

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