title: Involvement of cystic fibrosis transmembrane conductance regulator (CFTR) in the pathogenesis of hydrosalpinx induced by Chlamydia trachomatis infection.
abstract: BACKGROUND
  Genital Chlamydia (C) trachomatis infection has been recognized as the single most common cause of pelvic inflammatory disease leading to severe tubal damage, ectopic pregnancy, infertility and hydrosalpinx. However, the mechanism underlying the formation of hydrosalpinx induced by C. trachomatis infection remains largely unknown. We performed this study to determine the involvement of cystic fibrosis transmembrane conductance regulator (CFTR), a cAMP-activated chloride channel that regulates epithelial electrolyte and fluid secretion, in hydrosalpinx fluid formation.
  
  
  METHODS
  Western blot analysis was used to determine CFTR expression in the hydrosalpinges that were seen on the ultrasound scans of infertile assisted reproduction treatment patients. Correlation with C. trachomatis infection was done by testing patients' sera for C. trachomatis immunoglobulin G antibody titer using a Capita enzyme-linked immunosorbent assay based kit. CFTR involvement was further verified in a rat C. trachomatis infection model and confirmed using CFTR mutant (CFTR(tm1Unc)) mice.
  
  
  RESULTS
  Here we report on the up-regulated expression of CFTR in the hydrosalpinx tissues of infertile patients with detectable serum levels of C. trachomatis antibody (immunoglobulin G). In a rat model, increased CFTR expression and fluid accumulation could be observed in the uterine horns infected with C. trachomatis elementary bodies, which was reversed by antibiotics treatment. In C. trachomatis-infected CFTR(tm1Unc) mice, however, no detectable fluid accumulation was observed.
  
  
  CONCLUSIONS
  These findings suggest the involvement of CFTR in the pathogenesis of hydrosalpinx fluid formation and may provide grounds for a better treatment strategy to improve assisted reproduction treatment outcome in infertile patients with hydrosalpinx.
authors.affiliation: Epithelial Cell Biology Research Center, Department of Physiology, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, China.
authors.forename: Louis Chukwuemeka
authors.initials: LC
authors.lastname: Ajonuma
authors.forename: Paul Kay Sheung
authors.initials: PK
authors.lastname: Chan
authors.forename: Ernest Hung Yu
authors.initials: EH
authors.lastname: Ng
authors.forename: Kin Lam
authors.initials: KL
authors.lastname: Fok
authors.forename: Connie Hau Yan
authors.initials: CH
authors.lastname: Wong
authors.forename: Lai Ling
authors.initials: LL
authors.lastname: Tsang
authors.forename: Xiao Xiao
authors.initials: XX
authors.lastname: Tang
authors.forename: Lok Sze
authors.initials: LS
authors.lastname: Ho
authors.forename: Miu Ching
authors.initials: MC
authors.lastname: Lau
authors.forename: Chin Man
authors.initials: CM
authors.lastname: Chung
authors.forename: Qiong
authors.initials: Q
authors.lastname: He
authors.forename: Hong Yi
authors.initials: HY
authors.lastname: Huang
authors.forename: Dong Zi
authors.initials: DZ
authors.lastname: Yang
authors.forename: Dewi Kenneth
authors.initials: DK
authors.lastname: Rowlands
authors.forename: Yiu Wa
authors.initials: YW
authors.lastname: Chung
authors.forename: Hsiao Chang
authors.initials: HC
authors.lastname: Chan
mesh_terms: D000328:Adult; D000818:Animals; D000907:Antibodies, Bacterial / Q000097:blood; D002690:Chlamydia Infections / Q000378:metabolism* / Q000382:microbiology; D002692:Chlamydia trachomatis / Q000302:isolation & purification*; D019005:Cystic Fibrosis Transmembrane Conductance Regulator / Q000378:metabolism*; D004195:Disease Models, Animal; D005184:Fallopian Tube Diseases / Q000378:metabolism* / Q000382:microbiology*; D005260:Female; D006801:Humans; D051379:Mice; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D000907:Antibodies, Bacterial; D019005:Cystic Fibrosis Transmembrane Conductance Regulator