The CD14 functional gene polymorphism -260 C&gt;T is not involved in either the susceptibility to Chlamydia trachomatis infection or the development of tubal pathology

Ouburg, Sander; Spaargaren, Joke; Hartog, J.E. den; Land, Jolande A.; Fennema, J. S. A.; Pleijster, Jolein; Peña, Amado Salvador; Morré, Servaas A.

doi:10.1186/1471-2334-5-114

Cited by 28 publications

(26 citation statements)

References 52 publications

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“…Limited studies conducted in Dutch Caucasian women examining for human genetic functional polymorphisms related to the innate immune molecules, TLR4 73, the LPS sensing TLR4 co-receptor CD14 74, IL-1β, and the IL-1 receptor 75 have so far revealed no association of functional polymorphisms in genes for these molecules and tubal infertility. In contrast, wild-type homozygosity for mannose-binding lectin (MBL) allele A has been associated with protection against tubal occlusion in Hungarian Caucasian women 76.…”

Section: What Is the Role Of Host Factors In Pathogenesis? Are There mentioning

confidence: 99%

Pathogenesis of Genital Tract Disease Due toChlamydia trachomatis

2010

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Although the pathologic consequences of C. trachomatis genital infection are well-established, the mechanism(s) that result in chlamydia-induced tissue damage are not fully understood. We have reviewed in vitro, animal, and human data related to the pathogenesis of chlamydial disease in an effort to better understand how reproductive sequelae result from C. trachomatis infection. Abundant in vitro data suggest the inflammatory response to chlamydiae is initiated and sustained by actively infected non-immune host epithelial cells. The mouse model indicates a critical role for chlamydia-activation of the innate immune receptor, toll-like receptor 2 (TLR2), and subsequent inflammatory cell influx and activation which contributes to the development of chronic genital tract tissue damage. Data from recent vaccine studies in the murine model and from human immunoepidemiologic studies support a role for chlamydia-specific CD4 Th1-IFN-γ-producing cells in protection from infection and disease. However, limited evidence obtained using animal models of repeated infection indicates that while the adaptive T cell response is a key mechanism involved in controlling or eliminating infection, it may have a double-edged nature, and contribute to tissue damage. Important immunologic questions include whether anamnestic CD4 T cell responses drive disease rather than protect against disease, and the role of specific immune cells and inflammatory mediators in the induction of tissue damage with primary and repeated infections. Continued study of the complex molecular and cellular interactions between chlamydiae and their host, and large-scale prospective immunoepidemiologic and immunopathologic studies are needed to address gaps in our understanding of pathogenesis, which thwart development of optimally effective control programs including vaccine development.

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Section: What Is the Role Of Host Factors In Pathogenesis? Are There mentioning

confidence: 99%

Pathogenesis of Genital Tract Disease Due toChlamydia trachomatis

2010

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“…Characteristics are described elsewhere [18]. In short, cervical swabs were taken and serum was collected from women attending an STI outpatient clinic in Amsterdam, the Netherlands.…”

Section: Methodsmentioning

confidence: 99%

Serovar D and E of serogroup B induce highest serological responses in urogenital Chlamydia trachomatisinfections

et al. 2014

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BackgroundChlamydia trachomatis is the most prevalent bacterial sexually transmitted infection (STI) worldwide. A strong link between C. trachomatis serogroup/serovar and serological response has been suggested in a previous preliminary study. The aim of the current study was to confirm and strengthen those findings about serological IgG responses in relation to C. trachomatis serogroups and serovars.MethodsThe study population (n = 718) consisted of two patient groups with similar characteristics of Dutch STI clinic visitors. We performed genotyping of serovars and used titre based and quantitative commercially available ELISA kits (medac Diagnostika) to determine specific serum IgG levels. Optical density (OD) values generated by both tests were used to calculate the IgG titres (cut-off 1:50). Analyses were conducted stratified by gender.ResultsWe observed very significant differences when comparing the median IgG titres of three serogroups, B, C and I: in women for B vs. C: p < 0.0001 (median titres B 200 vs. C <50); B vs. I: p < 0.0001 (200 vs. 50), and in men for B vs. C: p = 0.0006 (150 vs. <50); B vs. I: p = 0.0001 (150 vs. <50); C vs. I was not significant for both sexes. Serovars D and E of serogroup B had the highest median IgG titres compared to the other serovars in both men and women: 200 and 200 vs. ≤ 100 for women and 100 and 200 vs. ≤ 75 for men, respectively.ConclusionsThis study shows that B group serovars induce higher serological responses compared to the C and I group serovars in vivo in both men and women.

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“…36 Host genetic markers seem to be the most promising biological indicators of complicated chlamydia infection at present. [38][39][40][41][42][43][44][45][46][47] Recent studies have pioneered in identifiying genetic biomarkers useful to distinguish (i) women with a past chlamydia infection and higher probability to develop complications from (ii) women with an uncomplicated chlamydia infection cleared without late complications. The relevance of studying host genetic markers…”

Section: Accepted Articlementioning

confidence: 99%

Host factors and genetic susceptibility to infections due to intracellular bacteria and fastidious organisms

Asner¹,

Morré

Bochud³

et al. 2014

Clinical Microbiology and Infection

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While genetic polymorphisms play a paramount role in tuberculosis (TB), less is known about their contribution to the severity of diseases caused by other intracellular bacteria and fastidious microorganisms. We searched electronic databases for observational studies reporting on host factors and genetic predisposition to infections caused by intracellular fastidious bacteria published up to 30 May 2014. The contribution of genetic polymorphisms was documented for TB. This includes genetic defects in the mononuclear phagocyte/T helper cell type 1 (Th1) pathway contributing to disseminated TB disease in children and genome-wide linkage analysis (GWAS) in reactivated pulmonary TB in adults. Similarly, experimental studies supported the role of host genetic factors in the clinical presentation of illnesses resulting from other fastidious intracellular bacteria. These include IL-6 -174G/C or low mannose-binding (MBL) polymorphisms, which are incriminated in chronic pulmonary conditions triggered by C. pneumoniae, type 2-like cytokine secretion polymorphisms, which are correlated with various clinical patterns of M. pneumoniae infections, and genetic variation in the NOD2 gene, which is an indicator of tubal pathology resulting from Chamydia trachomatis infections. Monocyte/macrophage migration and T lymphocyte recruitment defects are corroborated to ineffective granuloma formation observed among patients with chronic Q fever. Similar genetic polymorphisms have also been suggested for infections caused by T. whipplei although not confirmed yet. In conclusion, this review supports the paramount role of genetic factors in clinical presentations and severity of infections caused by intracellular fastidious bacteria. Genetic predisposition should be further explored through such as exome sequencing.

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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

Cited by 28 publications

References 52 publications

Pathogenesis of Genital Tract Disease Due toChlamydia trachomatis

Pathogenesis of Genital Tract Disease Due toChlamydia trachomatis

Serovar D and E of serogroup B induce highest serological responses in urogenital Chlamydia trachomatisinfections

Host factors and genetic susceptibility to infections due to intracellular bacteria and fastidious organisms

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