Cytokine gene polymorphism and Chlamydia trachomatis-specific immune responses

Öhman, Hanna; Tiitinen, Aila; Halttunen, Mervi; Paavonen, Jorma; Surcel, Heljä‐Marja

doi:10.1016/j.humimm.2010.12.012

Cited by 22 publications

(19 citation statements)

References 35 publications

(50 reference statements)

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“…The HLA alleles and IL-10 allele were more frequently identified in the chlamydial tubal factor cohort than in the controls; however, the lymphocyte proliferation in response to cHSP60 was not significantly different in relation to the alleles (118). However, in a different study, distinct IL-10 and IFN-␥ polymorphisms were found to have a significant impact on lymphocyte proliferation in response to chlamydial antigens (119).…”

Section: Human Genotypic Factors Associated With C Trachomatis Infermentioning

confidence: 91%

Human and Pathogen Factors Associated with Chlamydia trachomatis-Related Infertility in Women

et al. 2015

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SUMMARY Chlamydia trachomatis is the most common bacterial sexually transmitted pathogen worldwide. Infection can result in serious reproductive pathologies, including pelvic inflammatory disease, ectopic pregnancy, and infertility, in women. However, the processes that result in these reproductive pathologies have not been well defined. Here we review the evidence for the human disease burden of these chlamydial reproductive pathologies. We then review human-based evidence that links Chlamydia with reproductive pathologies in women. We present data supporting the idea that host, immunological, epidemiological, and pathogen factors may all contribute to the development of infertility. Specifically, we review the existing evidence that host and pathogen genotypes, host hormone status, age of sexual debut, sexual behavior, coinfections, and repeat infections are all likely to be contributory factors in development of infertility. Pathogen factors such as infectious burden, treatment failure, and tissue tropisms or ascension capacity are also potential contributory factors. We present four possible processes of pathology development and how these processes are supported by the published data. We highlight the limitations of the evidence and propose future studies that could improve our understanding of how chlamydial infertility in women occurs and possible future interventions to reduce this disease burden.

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Section: Human Genotypic Factors Associated With C Trachomatis Infermentioning

confidence: 91%

Human and Pathogen Factors Associated with Chlamydia trachomatis-Related Infertility in Women

et al. 2015

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“…About 50% of infected men and 70 to 75% of infected women are asymptomatic. The infection is transmitted during sexual contact and to the newborn at birth and may cause neonatal conjunctivitis or pneumonia (5,6,(8)(9)(10) . Over 100 million individuals of both sexes worldwide are infected with Chlamydia at some point in their lives (6,9,10) .…”

Section: Introductionmentioning

confidence: 99%

“…Worldwide, it occurs more frequently in sexually active young adults, generally aged younger than 20 years, and it is nearly three times higher in the 14-24 years age group (5,7,9,10) . It currently represents the leading cause of female infertility, but the most common infections are urethritis and cervicitis, which, if untreated, can lead to serious consequences in the reproductive tract such as ectopic pregnancy and infertility (6,(8)(9)(10) . About 50% of infected men and 70 to 75% of infected women are asymptomatic.…”

Section: Introductionmentioning

confidence: 99%

“…

ARTICLE

INTRODUCTIONThe WHO estimates that there are 105.7 million new cases of Chlamydia worldwide, with 3 to 4 million of these only in the United States of America (USA), with over 1.4 million cases reported in 2011 (1)(2)(3)(4)(5) , 5 million in Eastern Europe, and 34 million in subSaharan Africa and southeast Asia (5)(6)(7)(8)(9) . Worldwide, it occurs more frequently in sexually active young adults, generally aged younger than 20 years, and it is nearly three times higher in the 14-24 years age group (5,7,9,10) .

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confidence: 99%

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Detection of chlamydia trachomatis by immunological methods in adult and adolescent female population in Cuiabá, Mato Grosso

Matos¹,

Machado²,

Zavala³

et al. 2015

J Bras Doenças Sex Transm

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ARTICLE INTRODUCTIONThe WHO estimates that there are 105.7 million new cases of Chlamydia worldwide, with 3 to 4 million of these only in the United States of America (USA), with over 1.4 million cases reported in 2011 (1)(2)(3)(4)(5) , 5 million in Eastern Europe, and 34 million in subSaharan Africa and southeast Asia (5)(6)(7)(8)(9) . Worldwide, it occurs more frequently in sexually active young adults, generally aged younger than 20 years, and it is nearly three times higher in the 14-24 years age group (5,7,9,10) . It currently represents the leading cause of female infertility, but the most common infections are urethritis and cervicitis, which, if untreated, can lead to serious consequences in the reproductive tract such as ectopic pregnancy and infertility (6,(8)(9)(10) . About 50% of infected men and 70 to 75% of infected women are asymptomatic. The infection is transmitted during sexual contact and to the newborn at birth and may cause neonatal conjunctivitis or pneumonia (5,6,(8)(9)(10) . Over 100 million individuals of both sexes worldwide are infected with Chlamydia at some point in their lives (6,9,10) . Among male subjects, the prevalence is comparable with that of risk populations, ranging from 15 to 20%, while in the asymptomatic population, it is between 3 and 7%. In female subjects, the infection rates of asymptomatic populations are between 3 and 10%, while in high-risk populations they are above 20% (1)

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“…These same cytokines, however, may also be implicated in disease pathogenesis. For many pathogens, including C. trachomatis, IFN plays an important role in resolution of infection (Marks, Tam et al 2010;Agrawal, Bhengraj et al 2011;Matthews, Wilkinson et al 2011;Ohman, Tiitinen et al 2011;Patel, Stefanidou et al 2011). The role of IFN in chlamydial clearance is complicated by the fact that inflammation can damage host cells and IFN itself can also drive persistence (Beatty, Belanger et al 1994).…”

Section: Introductionmentioning

confidence: 99%

Host-Pathogen Co-Evolution: Chlamydia trachomatis Modulates Surface Ligand Expression in Genital Epithelial Cells to Evade Immune Recognition

Caesar¹,

Ibana²,

Schust³

2012

Chlamydia

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Chlamydia 26infectious spill into the female peritoneal cavity. The disease can result in scarring and pelvic organ disfigurement that lead to increases in ectopic pregnancy rates, tubal factor infertility (Hellstrom, Schachter et al. 1987) and possibly early pregnancy wastage (Witkin 1999). If left untreated during pregnancy, chlamydial genital infections in women have been associated with preterm delivery (Rours, Duijts et al. 2011). Developmental cycle of Chlamydia trachomatisChlamydia exhibits a predominantly biphasic developmental cycle, differentiating between a metabolically inactive but infectious elementary body (EB) and a replicating and metabolically active, but non-infectious, reticulate body (RB) (Nelson, Virok et al. 2005;Linhares and Witkin 2010). Attachment and entry of EBs into permissive cells are critical steps in chlamydial development, but the molecules and mechanisms utilized in these processes are not well understood. Several bacterial ligands have been implicated as adhesins, and include heparin sulfate-like proteins, MOMP, OmcB, glycoproteins and Hsp70 (reviewed by Hackstadt 1999). The host factor/s involved in attachment is/are likely proteinacious, and the host cytoplasmic chaperone protein disulfide isomerase (PDI) has been strongly implicated as a structural requirement for attachment of multiple serovars, as well as necessary for entry (Davis, Raulston et al. 2002;Conant and Stephens 2007;Abromaitis and Stephens 2009). After EB internalization, Chlamydia-derived vesicles mature into a specialized parasitophorous vacuole termed an inclusion, which is nonfusogenic with lysosomal and endosomal membranes (Fields, Fischer et al. 2002;Carabeo, Mead et al. 2003;Hybiske and Stephens 2007a;Hybiske and Stephens 2007b). The exact mechanisms involved in the differentiation of the chlamydial EB into a RB remain incompletely described, but morphological investigations have demonstrated decondensation of chromatin occurs early in the process and supports the transition from a metabolically inert EB to a metabolically active RB (Beatty, Byrne, et al. 1993;Beatty, Morrison, et al. 1995;Belland, Zhong et al. 2003) Elegant investigations using transcriptional profiling have listed chaperonin, metabolite translocation, metabolite interconversion, endosomal trafficking, and inclusion membrane modification genes to be among the first to be activated (immediate early genes) during this transition (Belland, Zhong, et al. 2003;AbdelRahman and Belland 2005). As might have been predicted, these genes fall into categories required for pathogen acquisition of nutrients and for inhibiting fusion of the chlamydial inclusion with the host cell lysosomal pathway. Inside the inclusion, the elementary bodies differentiate into reticulate bodies that, in turn, divide rapidly via binary fission. RB condense back into EB and completion of the chlamydial cell cycle results in EB release by host cell lysis or extrusion (Todd and Caldwell 1985; ;Hybiske and Stephens 2007b). Secondary differentiation of RB back into EB invo...

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Cytokine gene polymorphism and Chlamydia trachomatis-specific immune responses

Cited by 22 publications

References 35 publications

Human and Pathogen Factors Associated with Chlamydia trachomatis-Related Infertility in Women

Human and Pathogen Factors Associated with Chlamydia trachomatis-Related Infertility in Women

Detection of chlamydia trachomatis by immunological methods in adult and adolescent female population in Cuiabá, Mato Grosso

Host-Pathogen Co-Evolution: Chlamydia trachomatis Modulates Surface Ligand Expression in Genital Epithelial Cells to Evade Immune Recognition

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