title: Interaction between CD14-159C>T polymorphism and Helicobacter pylori is associated with serum total immunoglobulin E.
abstract: 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.
  
  
  CONCLUSIONS
  Our results further emphasize the role of gene-environment interaction in the regulation of serum total IgE.
authors.affiliation: Department of Microbiology and Immunology, University of Tampere Medical School, Tampere, Finland. miia.virta@uta.fi
authors.forename: M
authors.initials: M
authors.lastname: Virta
authors.forename: T
authors.initials: T
authors.lastname: Pessi
authors.forename: M
authors.initials: M
authors.lastname: Helminen
authors.forename: T
authors.initials: T
authors.lastname: Seiskari
authors.forename: A
authors.initials: A
authors.lastname: Kondrashova
authors.forename: M
authors.initials: M
authors.lastname: Knip
authors.forename: H
authors.initials: H
authors.lastname: Hyöty
authors.forename: M
authors.initials: M
authors.lastname: Hurme
mesh_terms: D000293:Adolescent; D000483:Alleles; D019943:Amino Acid Substitution; D000818:Animals; D000907:Antibodies, Bacterial / Q000097:blood; D002353:Carrier State / Q000276:immunology*; D002648:Child; D005260:Female; D016481:Helicobacter Infections / Q000097:blood / Q000276:immunology*; D016480:Helicobacter pylori / Q000276:immunology*; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood* / Q000235:genetics; D018950:Lipopolysaccharide Receptors / Q000235:genetics*; D008297:Male; D020641:Polymorphism, Single Nucleotide; D051197:Toll-Like Receptor 4 / Q000235:genetics*; D014123:Toxoplasmosis / Q000097:blood / Q000235:genetics
chemical_list: D000907:Antibodies, Bacterial; D018950:Lipopolysaccharide Receptors; C495345:TLR4 protein, human; D051197:Toll-Like Receptor 4; D007073:Immunoglobulin E