Influence of a mannose-binding lectin gene polymorphism and exposure to Chlamydia trachomatis on fallopian tube obstruction in Brazilian woman
Carregando...
Citações na Scopus
0
Tipo de produção
article
Data de publicação
2019
Título da Revista
ISSN da Revista
Título do Volume
Editora
SPRINGER HEIDELBERG
Citação
ARCHIVES OF GYNECOLOGY AND OBSTETRICS, v.300, n.3, p.641-645, 2019
Resumo
Purpose Factors influencing fallopian tube occlusion in women with a lower genital tract infection remain incompletely elucidated. We evaluated whether a polymorphism in the mannose-binding lectin (MBL) gene at codon 54 influences the occurrence of fallopian tube blockage in relation to exposure to Chlamydia trachomatis. Methods In a case-control study at The Hospital das Clinicas, University of Sao Paulo, Brazil, 75 women with hysterosalpingography-documented tubal occlusion and 75 women with patent fallopian tubes were analyzed for detection of single-nucleotide polymorphism in codon 54 of the MBL gene and for IgG anti-C. trachomatis antibodies in their sera. Both groups were matched for age, race, and sexual variables. Results Prior exposure to C. trachomatis, as evidenced by the presence of IgG antibodies, was comparable in both groups. Detection of the polymorphic MBL allele was more prevalent in women with blocked tubes (p < 0.01), regardless of whether or not there was evidence of prior chlamydial exposure. Conclusion The level of MBL-related innate immunity influences the consequences of infection by C. trachomatis or other microbes.
Palavras-chave
Chlamydia trachomatis, Fallopian tube occlusion, Genetic polymorphism, Innate immunity, Mannose-binding lectin
Referências
- Babula O, 2004, AM J OBSTET GYNECOL, V191, P762, DOI 10.1016/j.ajog.2004.03.073
- Babula O, 2003, CLIN INFECT DIS, V37, P733, DOI 10.1086/377234
- Brunham RC, 2005, J INFECT DIS, V192, P1836, DOI 10.1086/497341
- Debattista J, 2003, FERTIL STERIL, V79, P1273, DOI 10.1016/S0015-0282(03)00396-0
- Exacoustos C, 2009, J MINIM INVAS GYN, V16, P437, DOI 10.1016/j.jmig.2009.03.019
- Garred P, 2006, GENES IMMUN, V7, P85, DOI 10.1038/sj.gene.6364283
- HALBRECHT I, 1946, LANCET, V250, P235
- Ip WKE, 2009, IMMUNOL REV, V230, P9, DOI 10.1111/j.1600-065X.2009.00789.x
- Wojitani MDKH, 2012, ARCH GYNECOL OBSTET, V285, P149, DOI 10.1007/s00404-011-1920-z
- Klein NJ, 2005, MOL IMMUNOL, V42, P919, DOI 10.1016/j.molimm.2004.12.006
- Kodaman PH, 2004, CURR OPIN OBSTET GYN, V16, P221, DOI 10.1097/01.gco.0000129421.98370.0d
- Linhares IM, 2010, CELL STRESS CHAPERON, V15, P467, DOI 10.1007/s12192-010-0171-4
- Mardh PA, 2004, CURR OPIN INFECT DIS, V17, P49, DOI 10.1097/01.qco.0000113650.87656.a8
- Perquin DAM, 2007, FERTIL STERIL, V88, P224, DOI 10.1016/j.fertnstert.2006.11.078
- Swanson AF, 1998, INFECT IMMUN, V66, P1607
- Sziller I, 2007, HUM REPROD, V22, P1861, DOI 10.1093/humrep/dem107
- Tsevat DG, 2017, AM J OBSTET GYNECOL, V216, P1, DOI 10.1016/j.ajog.2016.08.008
- Turner MW, 2004, NETH J MED, V62, P4