title: The -159 C-->T polymorphism of CD14 is associated with nonatopic asthma and food allergy.
abstract: BACKGROUND
  CD14, the receptor for LPS, plays an important role in innate immunity. A polymorphism in the promotor for CD14, -159 C-->T, has been implicated in atopy.
  
  
  OBJECTIVE
  We explored the relationship of this polymorphism with both atopic and nonatopic asthma, as well as with food allergy.
  
  
  METHODS
  Patients with asthma and food allergy were recruited along with nonatopic, nonasthmatic control subjects. The -159 C-->T polymorphism was genotyped by using the PCR-based RFLP assay.
  
  
  RESULTS
  The -159 T allele was more common among patients with nonatopic asthma and food allergy than among control subjects (chi(2) = 6.03, P =.01 and chi(2) = 4.94; P =.03, respectively). Patients with food allergy had a 4-fold increased odds of having the TT genotype versus carriers of the C allele compared with control subjects (odds ratio [OR] = 3.9, 95% CI = 1.5-10.3), whereas patients with nonatopic asthma had a 3-fold increased odds of having the TT genotype (OR = 3.1 [95% CI = 1.1-9.1]). Controlling for sex differences between groups did not alter this relationship, which remained significant for patients with food allergy (OR = 3.7 [95% CI = 1.4-10.1]) or nonatopic asthma (OR = 2.7 [95% CI = 0.9-8.0]). We performed a stratified analysis, limited to white patients, to reduce population stratification. The relationship with the TT genotype was stronger in white patients with nonatopic asthma (OR = 4.4 [95% CI = 1.3-14.8]) and patients with food allergy (OR = 5.1 [95% CI = 1.6-16.2]), even adjusting for sex differences (OR = 3.9 [95% CI = 1.1-13.5] and OR = 4.6 [95% CI = 1.4-14.8], respectively).
  
  
  CONCLUSIONS
  The TT genotype of -159 C-->T CD14 is associated with nonatopic asthma and food allergy, particularly in white subjects. Thus CD14 is a candidate gene specifically for nonatopic asthma and not for asthma in general. This indicates that atopic and nonatopic asthma might be distinct conditions in their genetic predisposition, despite the fact that they are very similar once they have been established.
authors.affiliation: Division of Epidemiology and Biostatistics, Department of Environmental Health, University of Cincinnati Medical Center, Ohio, USA.
authors.forename: Jessica G
authors.initials: JG
authors.lastname: Woo
authors.forename: Amal
authors.initials: A
authors.lastname: Assa'ad
authors.forename: Angela B
authors.initials: AB
authors.lastname: Heizer
authors.forename: Jonathan A
authors.initials: JA
authors.lastname: Bernstein
authors.forename: Gurjit K Khurana
authors.initials: GK
authors.lastname: Hershey
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001249:Asthma / Q000235:genetics*; D002648:Child; D002675:Child, Preschool; D003596:Cytosine; D005260:Female; D005512:Food Hypersensitivity / Q000235:genetics*; D005838:Genotype; D006801:Humans; D007223:Infant; D018950:Lipopolysaccharide Receptors / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D016017:Odds Ratio; D016133:Polymerase Chain Reaction; D012150:Polymorphism, Restriction Fragment Length; D020641:Polymorphism, Single Nucleotide; D012727:Sex Characteristics; D013941:Thymine; D044465:White People / Q000235:genetics
chemical_list: D018950:Lipopolysaccharide Receptors; D003596:Cytosine; D013941:Thymine