Interaction between CD14−159C>T polymorphism and Helicobacter pylori is associated with serum total immunoglobulin E

• Published in: Clinical & Experimental Allergy
• Main Authors: Virta, M., Pessi, T., Helminen, M., Seiskari, T., Kondrashova, A., Knip, M., Hyöty, H., Hurme, M.
• Format: Article in Journal/Newspaper
• Language: English
• Published: Wiley 2008
• Subjects: karelia*; karelian
• Online Access: http://dx.doi.org/10.1111/j.1365-2222.2008.03103.x; https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1111%2Fj.1365-2222.2008.03103.x; https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1365-2222.2008.03103.x

Summary Background Total serum IgE is regulated by both environmental and genetic factors. Association and linkage studies have suggested a role of CD14 −159C>T polymorphism in the regulation of serum total IgE, but the results have been contradictory. It seems that gene–environment interactions are involved in this regulation. Objective The aim of this study was to examine the possible gene–environment interactions among Toxoplasma gondii, Helicobacter pylori, CD14 −159C>T and Toll‐like receptor (TLR) 4 +896A>G polymorphism on serum total IgE. For this study, we expanded the scope of our earlier comparison of allergic sensitization and microbial load between Finland and Russian Karelia by studying the CD14 −159C>T and TLR4 +896A>G polymorphism in a cohort of Russian Karelian children. Methods For this study, CD14 −159C>T and TLR4 +896A>G polymorphisms were analysed in 264 healthy Russian Karelian children. Serum total IgE levels and H. pylori and T. gondii antibodies were also measured. Results We constructed a multiway anova model to analyse the gene–environment interactions among T. gondii seropositivity, H. pylori seropositivity, CD14 −159C>T and TLR4 +896A>G polymorphisms on serum total IgE. The model showed that there was an interaction between the CD14 −159 allele T carrier status and H. pylori antibodies on serum total IgE ( P =0.004). No other interactions were found. Conclusion Our results further emphasize the role of gene–environment interaction in the regulation of serum total IgE.