Chlamydia trachomatis infection, Fallopian tube damage and a mannose-binding lectin codon 54 gene polymorphism

I. Sziller, O. Babula, A. Ujházy, B. Nagy, P. Hupuczi, Z. Papp, I. M. Linhares, W. J. Ledger, S. S. Witkin

Research output: Article

16 Citations (Scopus)


Background: Mannose-binding lectin (MBL), a component of the innate immune system, provides a first-line defense against invading microorganisms. Polymorphisms in the MBL gene have been associated with increased risk of infection. Chlamydia trachomatis genital tract infections are a major cause of Fallopian tube occlusion. Our objective was to test whether an MBL codon 54 polymorphism might contribute to development of C. trachomatis-associated tubal damage. Methods: In a case-control study, 97 women with occluded and 104 women with patent Fallopian tubes were tested for a history of chlamydial infection by serology and for their MBL codon 54 genotype by PCR and restriction fragment length polymorphism analysis. Clinical data were blinded to those performing all laboratory analyses. Results: Women with tubal occlusion who also had a positive chlamydial serology had the highest rate of variant MBL B allele carriage (P < 0.001). Among women who were chlamydial antibody negative, allele B carriage was also more frequent in those with blocked, as opposed to patent, Fallopian tubes (P < 0.01). Conclusions: Wild-type allele A homozygosity is protective against, while carriage of the variant allele B is a risk factor for, Fallopian tube occlusion in women who are seropositive or seronegative for C. trachomatis.

Original languageEnglish
Pages (from-to)1861-1865
Number of pages5
JournalHuman Reproduction
Issue number7
Publication statusPublished - júl. 2007

ASJC Scopus subject areas

  • Reproductive Medicine
  • Obstetrics and Gynaecology

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