Role of cervical dendritic cell subsets, co-stimulatory molecules, cytokine secretion profile and beta-estradiol in development of sequalae to Chlamydia trachomatis infection

Agrawal, Tanvi; Vats, Vikas; Wallace, Paul K.; Salhan, Sudha; Mittal, Aliza

doi:10.1186/1477-7827-6-46

Cited by 25 publications

(29 citation statements)

References 43 publications

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Section: Guinea Pig Modelsmentioning

confidence: 87%

“…It was shown that estradiol, but not progesterone, makes guinea pigs more susceptible to chlamydial infections (96,97). Human surveys show that estradiol has the same effect in women (98,99).In guinea pigs, both humoral and cell-mediated immunity are required for resolution of infection and immunity to reinfection (100-102). The immunity to reinfection that occurs in the animals is short lasting, which is also analogous to humans (103).…”

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confidence: 96%

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Animal Models for Studying Female Genital Tract Infection with Chlamydia trachomatis

2013

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Chlamydia trachomatis is a Gram-negative obligate intracellular bacterial pathogen. It is the leading cause of bacterial sexually transmitted disease in the world, with more than 100 million new cases of genital tract infections with C. trachomatis occurring each year. Animal models are indispensable for the study of C. trachomatis infections and the development and evaluation of candidate vaccines. In this paper, the most commonly used animal models to study female genital tract infections with C. trachomatis will be reviewed, namely, the mouse, guinea pig, and nonhuman primate models. Additionally, we will focus on the more recently developed pig model. Chlamydia trachomatis, a Gram-negative obligate intracellular bacterium, is the leading cause of bacterial sexually transmitted disease. World Health Organization values for 2008 estimated an annual increase of over 100 million genital tract infections with C. trachomatis worldwide (1). The incidence of cases is increasing in many countries (1, 2). Genital tract infections with C. trachomatis can cause cervicitis in women and urethritis in men. However, these infections remain largely subclinical in approximately 70% of women and 50% of men and consequently are often not detected (3). Untreated infections may lead to pelvic inflammatory disease, tubal scarring, ectopic pregnancy, infertility, and chronic pelvic pain in women, epididymitis in men, and infant pneumonia in children (4-7). Uncomplicated chlamydial infections can be treated easily with antibiotics, but once infection and pathology are established, treatment may be less effective. Asymptomatic individuals can be identified through screening programs, but this approach is likely to be too costly for developing countries. A vaccination program would be much cheaper and have a greater impact in controlling C. trachomatis infections worldwide. Computer modeling suggests that even a partially efficacious chlamydial vaccination program would rapidly reduce the prevalence of genital infection (8). Animal models are indispensable for the study of C. trachomatis infections and the development and evaluation of candidate vaccines. Various animal models have been developed, including mouse (9, 10), guinea pig (11, 12), nonhuman primate (13,14), pig (15), rat (16), and rabbit (17) models. Here, the most commonly used animal models to study female genital tract infections with C. trachomatis will be reviewed, namely, the mouse, guinea pig, and nonhuman primate models. Additionally, we will focus on the more recently developed pig model. MOUSE MODELSMice are the most commonly used animals to study genital chlamydial infections. The advantages of the mouse model are their small size, ease of handling, availability in sufficient amounts, and low cost. Moreover, there are many well-characterized inbred and knockout mouse strains available (18). The female mouse genital tract is susceptible to infection with both Chlamydia muridarum (9) and C. trachomatis (10), which has resulted in the establishment of two murine mod...

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Section: Guinea Pig Modelsmentioning

confidence: 87%

mentioning

confidence: 96%

Animal Models for Studying Female Genital Tract Infection with Chlamydia trachomatis

2013

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“…By inducing cervical metaplasia C trachomatis infection can provide target cells for acquisition of HPV (especially HPV type 18) 4 6. On the other hand, by causing local immunoperturbation it may interfere with immune surveillance of persistent infection with hrHPV types 9. These two alternatives are supported by cohort studies that show that C trachomatis infection is a risk factor for both incident hrHPV infection and persistence of hrHPV DNA 10–13.…”

Section: Introductionmentioning

confidence: 98%

Chlamydia trachomatis infection and risk of cervical intraepithelial neoplasia

Lehtinen

Ault

Lyytikainen

et al. 2011

Sexually Transmitted Infections

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ObjectivesHigh-risk human papillomavirus (hrHPV) is the primary cause of cervical cancer. As Chlamydia trachomatis is also linked to cervical cancer, its role as a potential co-factor in the development of cervical intraepithelial neoplasia (CIN) grade 2 or higher was examined.MethodsThe placebo arms of two large, multinational, clinical trials of an HPV6/11/16/18 vaccine were combined. A total of 8441 healthy women aged 15–26 years underwent cervicovaginal cytology (Papanicolaou (Pap) testing) sampling and C trachomatis testing at day 1 and every 12 months thereafter for up to 4 years. Protocol-specified guidelines were used to triage participants with Pap abnormalities to colposcopy and definitive therapy. The main outcome measured was CIN.ResultsAt baseline, 2629 (31.1%) tested positive for hrHPV DNA and 354 (4.2%) tested positive for C trachomatis. Among those with HPV16/18 infection (n=965; 11.4%) or without HPV16/18 infection (n=7382, 87.5%), the hazard ratios (HRs) associated with development of any CIN grade 2 according to baseline C trachomatis status were 1.82 (95% CI: 1.06 to 3.14) and 1.74 (95% CI 1.05 to 2.90), respectively. The results were comparable when only the 12 most common hrHPV infections were considered, but the excess risk disappeared when the outcome was expanded to include CIN grade 3 or worse.ConclusionFurther studies based on larger cohorts with longitudinal follow-up in relation to the C trachomatis acquisition and a thorough evaluation of temporal relationships of infections with hrHPV types, C trachomatis and cervical neoplasia are needed to demonstrate whether and how in some situations C trachomatis sets the stage for cervical carcinogenesis.Trial registrationNCT00092521 and NCT00092534.

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“…Although the mechanism by which CT induces cervical neoplasia is unknown, two theories have been proposed for its role as a risk factor in HPV-associated cervical cancer (139,140). Whereas some studies have shown that CT infection increases the susceptibility for HPV uptake (141), others have highlighted its role in increasing HPV infection persistence (142,143), thereby leading to cervical metaplasia. Increased levels of CT DNA or IgG antibodies were found in HPV-infected women, suggesting a common route for transmission and co-infection (144).…”

Section: Chlamydia Trachomatis (Ct) and Hpvmentioning

confidence: 99%

Multiple Infections and Cancer: Implications in Epidemiology

Vedham

Divi

Starks

et al. 2014

Technol Cancer Res Treat

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Approximately 18% of the global cancer burden has been attributed to infectious agents, with estimates ranging from 7% in developed countries to about 22% in developing countries.Chronic infections caused by the hepatitis B and C viruses, human papilloma viruses (HPV), and Helicobacter pylori (H. pylori) are reported to be responsible for approximately 15% of all human cancers. Interestingly, although many of the infectious agents that have been associated with cancer-such as HPV, Epstein-Barr virus (EBV), and H. pylori-are highly prevalent in the world, most infected individuals do not develop cancer but remain lifelong carriers. Malignancies associated with infectious agents may result from prolonged latency as a result of chronic infections. Pathogenic infections are necessary but are not sufficient for cancer initiation or progression. Cancer initiation may require additional cofactors, including secondary infections. Therefore, in patients with chronic infection with one agent, secondary co-infection with another agent may serve as an important co-factor that may cause cancer initiation and progression. Additionally, opportunistic co-infections could significantly inhibit response to cancer treatment and increase cancer mortality. Co-infections are relatively common in areas with a high prevalence of infectious agents, especially in developing countries. These co-infections can cause an imbalance in the host immune system by affecting persistence of and susceptibility to malignant infections. Several articles have been published that focus on infectious agents and cancer. In this article, we discuss the role of infectious agents in malignancies, highlight the role of multiple/co-infections in cancer etiology, and review implications for cancer epidemiology.

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Role of cervical dendritic cell subsets, co-stimulatory molecules, cytokine secretion profile and beta-estradiol in development of sequalae to Chlamydia trachomatis infection

Cited by 25 publications

References 43 publications

Animal Models for Studying Female Genital Tract Infection with Chlamydia trachomatis

Animal Models for Studying Female Genital Tract Infection with Chlamydia trachomatis

Chlamydia trachomatis infection and risk of cervical intraepithelial neoplasia

Multiple Infections and Cancer: Implications in Epidemiology

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