Chlamydia Trachomatis Infection-Associated Risk of Cervical Cancer

Zhu, Haiyan; Shen, Zefeng; Luo, Hui; Zhang, Wenwen; Zhu, Xueqiong

doi:10.1097/md.0000000000003077

Cited by 171 publications

(151 citation statements)

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“…CdtA and CdtC ensure the uptake and cellular delivery of CdtB, which harbours the catalytic activity of CDT and causes double-strand DNA breaks (DSBs) in host cells. After host cell binding and internalization by Salmonella Typhi Bacterium Gallbladder carcinoma [13] Salmonella Enteritidis Bacterium Colon carcinoma in the ascending and transverse parts of the colon [14] Chlamydia trachomatis Bacterium Carcinoma of the cervix and ovaries [104,105] particularly sensitive to these toxins. As a result, this toxin can locally eliminate immune cells, providing an obvious advantage for the bacteria.…”

Section: Bacterial Toxin-mediated Host Cell Transformationmentioning

confidence: 99%

Bacterial infections and cancer

2018

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Infections are estimated to contribute to 20% of all human tumours. These are mainly caused by viruses, which explains why a direct bacterial contribution to cancer formation has been largely ignored. While epidemiological data link bacterial infections to particular cancers, tumour formation is generally assumed to be solely caused by the ensuing inflammation responses. Yet, many bacteria directly manipulate their host cell in various phases of their infection cycle. Such manipulations can affect host cell integrity and can contribute to cancer formation. We here describe how bacterial surface moieties, bacterial protein toxins and bacterial effector proteins can induce host cell DNA damage, and thereby can interfere with essential host cell signalling pathways involved in cell proliferation, apoptosis, differentiation and immune signalling.

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Section: Bacterial Toxin-mediated Host Cell Transformationmentioning

confidence: 99%

Bacterial infections and cancer

2018

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“…12 The direct implication of C. trachomatis in the pathogenesis of malignancy has been highlighted in recent studies on women. It has been reported that C. trachomatis promotes HPV persistence, [13][14][15] suggesting that it should not be simply considered as a comorbidity of HPV infection, but should be regarded as an independent predictor of cervical cancer risk. Moreover, in young asymptomatic women the presence of C. trachomatis seems to significantly increase the risk of pre-cancer lesions.…”

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confidence: 99%

Chlamydia trachomatis and HPV co‐infections in HIV negative men from a multi‐ethnic area of Northern Italy at high prevalence of cervical malignancies

Comar

Monasta

Seraceni

et al. 2017

Journal of Medical Virology

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Chlamydia trachomatis and HPV coinfections in the male population are often a disregarded issue. We performed a study to evaluate the prevalence of such infections in heterosexual HIV negative men from a Northern Italy multi-ethnic area at high prevalence for cervical malignancies. Urethral swabs (US) or first-voided urine were evaluated retrospectively from 1317 patients attending Sexually Transmitted Infections (STI) clinic and from 3388 outpatients attending private clinics. Informations about participants' demographic characteristics and attributes of C. trachomatis, including chronic infection, and HPV genotypes testing, were collected. Exact Fisher test, bivariate, and multivariate logistic regressions were carried out. The prevalence of C. trachomatis was 1.7% in the outpatients and 16.9% in the STI group (P < 0.0001) in which the highest frequency was observed in men of age ≤25 years. Among patients with C. trachomatis, asymptomatic HPV co-infection was detected in 33% of men from the STI clinic and in 2% of the outpatients. Out of all coinfections, 56% were due to single HPV, with a prevalence of 73% in young STI men. The distribution of HPV genotypes confirmed the increased circulation of LR-HPV42, HR-HPV51, HR-HPV52 and prHR-HPV82, and the decreasing of HR-HPV16. African nationalities and leucorrhea were significantly associated risk factors, while the regular condom use offered an effective protection. This study highlights the high prevalence of C. trachomatis and HPV asymptomatic co-infection in young HIV negative men attending the STI clinic, representing a reservoir of new HPV genotypes with potential oncogenic risk.

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“…The intense interest in bacteria that induce DSBs in the host is driven largely by connections with carcinogenesis caused by enhanced genome instability. Helicobacter pylori infection is associated with stomach cancers (Hanada & Graham, ); Salmonella typhi is associated with gallbladder cancers (Koshiol et al., ); and Chlamydia trachomatis is associated with cervical cancers (Zhu, Shen, Luo, Zhang, & Zhu, ). Interestingly, all of these bacteria can introduce DSBs in host cells (Chumduri, Gurumurthy, Zadora, Mi, & Meyer, ; Grasso & Frisan, ; Hanada et al., ).…”

Section: Introductionmentioning

confidence: 99%

Aggregatibacter actinomycetemcomitans infection causes DNA double‐strand breaks in host cells

et al. 2018

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Periodontal disease, an inflammatory disease, is caused by infection with periodontal pathogens. Long-term periodontal disease increases the risk of oral carcinogenesis. Similar to other peptic cancers, oral carcinogenesis also requires multiple genome instabilities; however, the risk factors related to the accumulation of genome instabilities are poorly understood. Here, we suggested that specific periodontal pathogens may increase the risk of genome instability. Accordingly, we screened several periodontal pathogens based on the ability to induce DNA double-strand breaks (DSBs) in host cells. We found that Aggregatibacter actinomycetemcomitans Y4 infection induced DSB formation in host cells. To assess whether DSB formation induced by infection with A. actinomycetemcomitans occurred through apoptotic chromosome fragmentation, cells were treated with a caspase inhibitor, Z-VAD-FMK. DSB accumulation induced by infection with A. actinomycetemcomitans was observed, even in the presence of Z-VAD-FMK, suggesting that this breakage occurred independently of apoptosis. These results suggested that some periodontal pathogens can increase the risk of genome instabilities in host cells and subsequently increase the risk of carcinogenesis.

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Chlamydia Trachomatis Infection-Associated Risk of Cervical Cancer

Cited by 171 publications

References 50 publications

Bacterial infections and cancer

Bacterial infections and cancer

Chlamydia trachomatis and HPV co‐infections in HIV negative men from a multi‐ethnic area of Northern Italy at high prevalence of cervical malignancies

Aggregatibacter actinomycetemcomitans infection causes DNA double‐strand breaks in host cells

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