title: Human formyl peptide receptor 1 (FPR1) c.32C>T SNP is associated with decreased soluble E-selectin levels.
abstract: OBJECTIVE
  The human formyl peptide receptor (FPR) is a G protein-coupled chemoattractant receptor that is thought to mediate inflammatory responses. The FPR1 gene is highly polymorphic. In a recent study, the FPR1 c.32C>T SNP, resulting in the amino-acid substitution I11T, was reported to be significantly associated with C-reactive protein levels. Therefore, this study sought to determine if the impact of such a genetic variation extends to other clinical parameters associated with inflammation, including cytokines, adhesion molecules and inflammatory markers.
  
  
  METHODS
  This study was carried out on a subsample of 325 adults selected from the STANISLAS cohort study. The FPR1 c.32C>T SNP was genotyped using PCR amplification followed by restriction enzyme digestion. Anthropometric measurements and biochemical profiles were assessed for each individual.
  
  
  RESULTS
  The allele frequencies of FPR1 c.32C>T were 0.74 for the 32C allele and 0.26 for the 32T allele. Genotype frequencies were 0.55 for C/C, 0.38 for C/T and 0.07 for T/T. After adjusting for age, sex, BMI, alcohol and cigarette consumption, oral contraceptive, antibiotics and anti-inflammatory drug use, statistical analysis (under a recessive model of inheritance) demonstrated that serum E-selectin levels were 68% lower in individuals homozygous for T/T than in those with C/T or C/C genotypes (p = 0.001). However, no significant correlations were found for C-reactive protein or the other 18 tested clinical parameters that were analyzed in this study.
  
  
  CONCLUSIONS
  The FPR1 c.32C>T SNP may be associated with E-selectin levels in the French population. Although of importance, these findings need confirmation in larger studies.
authors.affiliation: Nancy-Université, Nancy, France.
authors.forename: Hamanou
authors.initials: H
authors.lastname: Benachour
authors.forename: Mohamed
authors.initials: M
authors.lastname: Zaiou
authors.forename: Bernard
authors.initials: B
authors.lastname: Herbeth
authors.forename: Daniel
authors.initials: D
authors.lastname: Lambert
authors.forename: John V
authors.initials: JV
authors.lastname: Lamont
authors.forename: Michèle
authors.initials: M
authors.lastname: Pfister
authors.forename: Gérard
authors.initials: G
authors.lastname: Siest
authors.forename: Laurence
authors.initials: L
authors.lastname: Tiret
authors.forename: Stefan
authors.initials: S
authors.lastname: Blankenberg
authors.forename: Peter S
authors.initials: PS
authors.lastname: Fitzgerald
authors.forename: Sophie
authors.initials: S
authors.lastname: Visvikis-Siest
mesh_terms: D000328:Adult; D000483:Alleles; D000886:Anthropometry; D015415:Biomarkers / Q000097:blood; D015331:Cohort Studies; D019040:E-Selectin / Q000097:blood*; D005260:Female; D005602:France; D005787:Gene Frequency; D005808:Genes, Recessive; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006720:Homozygote; D006801:Humans; D007249:Inflammation / Q000209:etiology; D008297:Male; D008875:Middle Aged; D008957:Models, Genetic; D020641:Polymorphism, Single Nucleotide; D044042:Receptors, Formyl Peptide / Q000235:genetics*; D012995:Solubility
chemical_list: D015415:Biomarkers; D019040:E-Selectin; C469986:FPR1 protein, human; D044042:Receptors, Formyl Peptide