title: The CD14 functional gene polymorphism -260 C>T is not involved in either the susceptibility to Chlamydia trachomatis infection or the development of tubal pathology.
abstract: BACKGROUND
  The functional polymorphism -260 C>T in the LPS sensing TLR4 co-receptor CD14 gene enhances the transcriptional activity and results in a higher CD14 receptor density. Individuals carrying the T/T genotype also have significantly higher serum levels of soluble CD14. The T allele of this polymorphism has recently been linked to Chlamydia pneumoniae infection. We investigated the role of the CD14 -260 C>T polymorphism in the susceptibility to and severity (defined as subfertility and/or tubal pathology) of C. trachomatis infection in Dutch Caucasian women.
  
  
  METHODS
  The different CD14 -260 C>T genotypes were assessed by PCR-based RFLP analysis in three cohorts: 1) A cohort (n = 576) of women attending a STD clinic, 2) a cohort (n = 253) of women with subfertility, and 3) an ethnically matched control cohort (n = 170). The following variables were used in the analysis: In cohort 1 the CT-DNA status, CT IgG serology status, self-reported symptoms and in cohort 2, the CT IgG serology status and the tubal status at laparoscopy.
  
  
  RESULTS
  In the control cohort the CC, CT and TT genotype distribution was: 28.2%, 48.2%, and 23.5% respectively. No differences were found in the overall prevalence of CD14 -260 genotypes (28.1%, 50.7%, and 21.2%) in cohort 1 when compared to the control cohort. Also no differences were observed in women with or without CT-DNA, with or without serological CT responses, with or without symptoms, or in combinations of these three variables. In subfertile women with tubal pathology (cohort 2, n = 50) the genotype distribution was 28.0%, 48.0%, and 24.0% and in subfertile women without tubal pathology (n = 203), 27.6%, 49.3% and 23.2%. The genotype distribution was unchanged when CT IgG status was introduced in the analyses.
  
  
  CONCLUSIONS
  The CD14 -260 C>T genotype distributions were identical in all three cohorts, showing that this polymorphism is not involved in the susceptibility to or severity of sequelae of C. trachomatis infection.
authors.affiliation: Department of Pathology, VU University Medical Centre, Amsterdam, The Netherlands. s.ouburg@vumc.nl
authors.forename: Sander
authors.initials: S
authors.lastname: Ouburg
authors.forename: Joke
authors.initials: J
authors.lastname: Spaargaren
authors.forename: Janneke E
authors.initials: JE
authors.lastname: den Hartog
authors.forename: Jolande A
authors.initials: JA
authors.lastname: Land
authors.forename: Johan S A
authors.initials: JS
authors.lastname: Fennema
authors.forename: Jolein
authors.initials: J
authors.lastname: Pleijster
authors.forename: A Salvador
authors.initials: AS
authors.lastname: Peña
authors.forename: Servaas A
authors.initials: SA
authors.lastname: Morré
mesh_terms: D000293:Adolescent; D000328:Adult; D016022:Case-Control Studies; D002690:Chlamydia Infections / Q000235:genetics / Q000382:microbiology* / Q000473:pathology*; D002692:Chlamydia trachomatis / Q000502:physiology*; D015331:Cohort Studies; D005184:Fallopian Tube Diseases / Q000235:genetics / Q000382:microbiology* / Q000473:pathology*; D005187:Fallopian Tubes / Q000473:pathology; D005260:Female; D020022:Genetic Predisposition to Disease / Q000235:genetics; D005838:Genotype; D006801:Humans; D018950:Lipopolysaccharide Receptors / Q000235:genetics*; D009426:Netherlands; D011110:Polymorphism, Genetic / Q000235:genetics*; D044465:White People
chemical_list: D018950:Lipopolysaccharide Receptors