Chlamydia trachomatis among sexually active teenage girls. Lack of correlation between chlamydial infection, history of the patient and clinical signs of infection

Rahm, Vivi-Anne; Gnarpe, Håkan; Odlind, Viveca

doi:10.1111/j.1471-0528.1988.tb06580.x

Cited by 56 publications

(26 citation statements)

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“…Untreated CT infections can lead to severe complications (Rahm, Gnarpe and Odlind 1988;Morre et al 2000), such as pelvic inflammatory disease (PID), ectopic pregnancy and tubal factor infertility (TFI) (Bjartling, Osser and Persson 2007;Price et al 2016). It has been estimated that 6.7% of a 35-year-old women who at least once tested positive for CT will develop TFI (Low et al 2006).…”

Section: Introductionmentioning

confidence: 99%

Performance of the multitarget Mikrogen Chlamydia trachomatis IgG ELISA in the prediction of tubal factor infertility (TFI) in subfertile women: comparison with the Medac MOMP IgG ELISA plus

Ess

Ouburg

Spaargaren

et al. 2017

Pathogens and Disease

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Performance of the multitarget Mikrogen Chlamydia trachomatis IgG ELISA in the prediction of tubal factor infertility (TFI) in subfertile women van Ess, Eleanne F.; Ouburg, Sander; Spaargaren, Joke; Land, Jolande A.; Morre, Servaas A. Take-down policy If you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediately and investigate your claim.Downloaded from the University of Groningen/UMCG research database (Pure): http://www.rug.nl/research/portal. For technical reasons the number of authors shown on this cover page is limited to 10 maximum. were respectively 32% (95% CI 26%-39%) and 30% (95% CI 24%-37%), and NPV 86% (95% CI 81%-91%) and 76% (95% CI 70%-82%). Both tests were comparable in the prediction of TFI. However, Mikrogen ELISA had a higher NPV and might be more reliable in identifying patients without TFI. Kappa-value showed limited concordance between both tests.

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Section: Introductionmentioning

confidence: 99%

Performance of the multitarget Mikrogen Chlamydia trachomatis IgG ELISA in the prediction of tubal factor infertility (TFI) in subfertile women: comparison with the Medac MOMP IgG ELISA plus

Ess

Ouburg

Spaargaren

et al. 2017

Pathogens and Disease

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“…Clinical data suggests that C. trachomatis evades immune-mediated elimination to cause persistent infections in some individuals (4,11,45,54,57,64,68). In women, chronic or recurrent C. trachomatis urogenital infections scar the Fallopian tubes, resulting in infertility and ectopic pregnancies, the two clinically important sequelae of infection (12,13).…”

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Murine Oviduct Epithelial Cell Cytokine Responses toChlamydia muridarumInfection Include Interleukin-12-p70 Secretion

2004

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Epithelial cells play an important role in host defense as sentinels for invading microbial pathogens.Chlamydia trachomatis is an intracellular bacterial pathogen that replicates in reproductive tract epithelium. Epithelial cells lining the reproductive tract likely play a key role in triggering inflammation and adaptive immunity during Chlamydia infections. For this report a murine oviduct epithelial cell line was derived in order to determine how epithelial cells influence innate and adaptive immune responses during Chlamydia infections. As expected, oviduct epithelial cells infected by Chlamydia muridarum produced a broad spectrum of chemokines, including CXCL16, and regulators of the acute-phase response, including interleukin-1␣ (IL-1␣), IL-6, and tumor necrosis factor alpha. In addition, infected epithelial cells expressed cytokines that augment gamma interferon (IFN) production, including IFN-␣/␤ and IL-12-p70. To my knowledge this is the first report of a non-myeloid/lymphoid cell type making IL-12-p70 in response to an infection. Equally interesting, infected epithelial cells significantly upregulated transforming growth factor alpha precursor expression, suggesting a mechanism by which they might play a direct role in the pathological scarring seen as a consequence of Chlamydia infections. Data from these in vitro studies predict that infected oviduct epithelium contributes significantly to host innate and adaptive defenses but may also participate in the immunopathology seen with Chlamydia infections.

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“…Chronic infection with urogenital serovars of C. trachomatis in the upper female reproductive tract can cause pelvic inflammatory disease (PID), scarring, and infertility (40,44,66). The ability of Chlamydia to cause a persistent infection suggests that the organism is able to effectively evade immune surveillance in some individuals (4,9,35,47,50,58,62). The initial innate immune response to Chlamydia infections results in the production of a plethora of cytokines and chemokines.…”

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Identifying a Role for Toll-Like Receptor 3 in the Innate Immune Response to Chlamydia muridarum Infection in Murine Oviduct Epithelial Cells

et al. 2012

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Because epithelial cells are the major cell type productively infected with Chlamydia during genital tract infections, the overall goal of our research was to understand the contribution of infected epithelial cells to the host defense. We previously showed that Toll-like receptor 3 (TLR3) is the critical pattern recognition receptor in oviduct epithelial (OE) cells that is stimulated during Chlamydia infection, resulting in the synthesis of beta interferon (IFN-␤). Here, we present data that implicates TLR3 in the expression of a multitude of other innate-inflammatory immune modulators including interleukin-6 (IL-6), CXCL10, CXCL16, and CCL5. We demonstrate that Chlamydia-induced expression of these cytokines is severely disrupted in TLR3-deficient OE cells, whereas Chlamydia replication in the TLR3-deficient cells is more efficient than in wild-type OE cells. Pretreatment of the TLR3-deficient OE cells with 50 U of IFN-␤/ml prior to infection diminished Chlamydia replication and restored the ability of Chlamydia infection to induce IL-6, CXCL10, and CCL5 expression in TLR3-deficient OE cells; however, CXCL16 induction was not restored by IFN-␤ preincubation. Our findings were corroborated in pathway-focused PCR arrays, which demonstrated a multitude of different inflammatory genes that were defectively regulated during Chlamydia infection of the TLR3-deficient OE cells, and we found that some of these genes were induced only when IFN-␤ was added prior to infection. Our OE cell data implicate TLR3 as an essential inducer of IFN-␤ and other inflammatory mediators by epithelial cells during Chlamydia infection and highlight the contribution of TLR3 to the inflammatory cytokine response.

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Chlamydia trachomatis among sexually active teenage girls. Lack of correlation between chlamydial infection, history of the patient and clinical signs of infection

Cited by 56 publications

References 10 publications

Performance of the multitarget Mikrogen Chlamydia trachomatis IgG ELISA in the prediction of tubal factor infertility (TFI) in subfertile women: comparison with the Medac MOMP IgG ELISA plus

Performance of the multitarget Mikrogen Chlamydia trachomatis IgG ELISA in the prediction of tubal factor infertility (TFI) in subfertile women: comparison with the Medac MOMP IgG ELISA plus

Murine Oviduct Epithelial Cell Cytokine Responses toChlamydia muridarumInfection Include Interleukin-12-p70 Secretion

Identifying a Role for Toll-Like Receptor 3 in the Innate Immune Response to Chlamydia muridarum Infection in Murine Oviduct Epithelial Cells

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