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Updated: Jul 15, 2026
09:11
A Human Fallopian Tube Model for Investigation of C. trachomatis Infections
Published on: August 11, 2012
Chlamydia trachomatis infection, Fallopian tube damage and a mannose-binding lectin codon 54 gene polymorphism.
I Sziller1, O Babula, A Ujházy
1First Department of Obstetrics and Gynecology, Faculty of Medicine, Semmelweis University, Baross utca 27, H-1088 Budapest, Hungary. sziller@noi1.sote.hu
Human Reproduction (Oxford, England)
|May 15, 2007
Summary
Mannose-binding lectin (MBL) gene variations are linked to Fallopian tube occlusion. The MBL variant allele B increases the risk of tubal damage, particularly in women with Chlamydia trachomatis infections.
Area of Science:
- Immunology
- Genetics
- Reproductive Health
Background:
- Mannose-binding lectin (MBL) is crucial for innate immunity against pathogens.
- MBL gene polymorphisms are associated with infection susceptibility.
- Chlamydia trachomatis infections frequently cause Fallopian tube occlusion.
Purpose of the Study:
- To investigate the association between MBL codon 54 polymorphism and Chlamydia trachomatis-associated tubal damage.
Main Methods:
- A case-control study involving 97 women with occluded and 104 with patent Fallopian tubes.
- Serological testing for Chlamydia trachomatis infection history.
- PCR and RFLP analysis for MBL codon 54 genotype.
Main Results:
- Women with tubal occlusion and positive Chlamydia trachomatis serology showed the highest MBL variant allele B carriage rate (P<0.001).
- Even in Chlamydia-seronegative women, MBL allele B was more frequent in those with Fallopian tube occlusion (P<0.01).
Conclusions:
- MBL wild-type allele A homozygosity appears protective against Fallopian tube occlusion.
- Carriage of the MBL variant allele B is a risk factor for Fallopian tube occlusion, irrespective of Chlamydia trachomatis serological status.
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