We evaluated the relationship of Chlamydia pneumoniae infection with prospective lung cancer risk using traditional serologic markers [microimmunoflourescence (MIF) IgG and IgA antibodies] and Chlamydia heat shock protein-60 (CHSP-60) antibodies, a marker for chronic chlamydial infection.
We conducted a nested case-control study (593 lung cancers and 671 controls) within the screening arm of the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial (N = 77,464). Controls were matched to cases by age, sex, randomization year, follow-up time, and smoking (pack-years of smoking, time since quitting). We assessed C. pneumoniae seropositivity and endpoint antibody titers (IgG and IgA against C. pneumoniae elementary bodies and IgG against CHSP-60).
C. pneumoniae seropositivity by microimmunoflourescence IgG or IgA antibodies was not associated with lung cancer [odds ratio of 0.88 and 95% confidence interval (95% CI) of 0.69-1.13 for IgG; odds ratio of 0.98 and 95% CI of 0.75-1.27 for IgA]. In contrast, individuals seropositive for CHSP-60 IgG antibodies had significantly increased lung cancer risk (odds ratio, 1.30; 95% CI, 1.02-1.67), and risk increased with increasing antibody titers (P trend = 0.006). CHSP-60-related risk did not differ significantly by lung cancer histology, follow-up time, or smoking. CHSP-60 seropositivity was associated with increased risk 2 to 5 years before lung cancer diagnosis (odds ratio, 1.77; 95% CI, 1.16-2.71; P trend = 0.006), thus arguing against reverse causality.
CHSP-60 seropositivity and elevated antibody titers were associated with significantly increased risk for subsequent lung cancer, supporting an etiologic role for C. pneumoniae infection in lung carcinogenesis.
Our results highlight the potential for lung cancer risk reduction through treatments targeted toward C. pneumoniae infections and chronic pulmonary inflammation.
"There is evidence for an association between infections with Salmonella typhi and cancer of the hepatic system . Other infections with bacteria such as Citrobacter rodentium in mice , Chlamydia pneumonia  and Streptococcus bovis  are likewise positively correlated with the incidence of malignancies. For these events, carcinogenesis represents the end point of a cascade in which bacterial toxin, inflammatory factors and mediators cause direct or indirect DNA damage that consecutively leads to cell transformation [7,13]. "
[Show abstract][Hide abstract] ABSTRACT: Different inflammatory processes may trigger the development of malignancies. Therefore, the aim of the present study was to evaluate a potential association between radiological determined chronic periodontitis (CPA) and oral squamous cell carcinoma (OSCC).
In a retrospective study, OSCC-patients and a control group without malignant tumors were radiographically examined for bone loss. Via telephone survey and questionnaire, general clinical data on the individual oral hygiene and concomitant diseases together with tobacco and alcohol use were assessed and data were compared between the groups.
178 OSCC-patients and 123 controls were included. In univariate analysis, a statistically relevant higher mean bone loss was seen in the OSCC group (4.3 mm (SD:1.8; 95% confidence interval (CI):4-4.6) vs. 2.9 mm (SD:0.7; 95% CI:2.8-3); p < 0.001)). This was confirmed in a multivariate regression model (OR:2.4, 95% CI:1.5-3.8; p < 0.001). A history of periodontal treatment was associated with significantly reduced OSCC risk (p < 0.001; OR:0.2, CI:0.1-0.5).
CPA is a common disease and the monitoring as well as the treatment of such a chronic oral inflammation may be beneficial in reducing one potential cause of OSCC. Therefore, further clinical studies on oral neoplasms should consider clinical periodontal parameters as well.
Head & Face Medicine 12/2013; 9(1):39. DOI:10.1186/1746-160X-9-39 · 0.85 Impact Factor
"Persons with elevated anti C. pneumoniae IgA antibody titers have up to a twofold increased risk for small cell carcinomas and adenocarcinomas of the lung and it is increased in male smoker patients with chronic C. pneumoniae infection  . Moreover, a significant association has been found with elevated Chlamydia Hsp-60 seropositivity, thus supporting an etiologic role of C. pneumoniae in lung carcinogenesis  . C. pneumoniae is also potent inducer of the proinflammatory cytokines TNF-a , IL-1b, and IL-6 in human monocytic cells, which may contribute to cancer development as demonstrated by the ability to activate PBMCs in vitro, and to grow inside these cells . "
[Show abstract][Hide abstract] ABSTRACT: The aetiology of OAL is undefined, although much attention has been recently focused on determining whether OAL is caused by an autoimmune disorder, chronic antigenic stimulation or both. It is becoming evident that infectious agents underlying chronic eye infection, as Chlamydia, may play a role in ocular lymphomagenesis. The high prevalence of Chlamydophila psittaci in patients with OAL has suggested a potential oncogenic role for its tendency to cause chronic and persistent infections, although it has been documented an evident geographical variability and response to antibiotic treatment. For C. pneumoniae, the findings so far obtained are very limited not only for identification in OAL but also for the specific treatment with antibiotics. The recent molecular and cultural evidence of C. trachomatis in patients with OAL, seems to suggest that also this pathogen may contribute to pathogenesis of such lymphoma. The potential appli- cation of bacteria-eradicating therapy at local and systemic level may ultimately result in safer and more efficient therapeutic option for patients affected by these malignancies. Moreover, a close collaboration between experts in oph- thalmology, infectious diseases and hematology will help, in the future, to effectively manage this disease. This review attempts to weigh the currently available evidence regarding the role that Chlamydia play in development of OAL and focuses on patients with OAL observed at our Institution.
Journal of Cancer Therapy 03/2013; 4(02):662-677. DOI:10.4236/jct.2013.42082
"Indeed, mycoplasma is one of the most often observed pathogen in lung carcinomas , and it has been postulated that mycoplasma-infected cells have a higher ability to metastasize in vivo than non-mycoplasma-infected cells . Very similarly, the bacterium Chlamydia pneumoniae, a common cause of community-acquired pneumonia, has been implicated in lung carcinogenesis [11-16]. Staphylococcus strains likewise have been observed in many cases of patients with lung cancer [6,7,17-19]. "
[Show abstract][Hide abstract] ABSTRACT: Clinical and experimental data suggest an association between the presence of bacterial and/or fungal infection and the development of different types of cancer, independently of chemotherapy-induced leukopenia. This has also been postulated for the development of lung cancer, however the prevalence and the exact species of the bacteria and fungi implicated, have not yet been described.
To determine the presence of bacterial and fungal microflora in surgically extracted samples of patients with lung cancer.
In this single-center prospective, observational study, tissue samples were surgically extracted from 32 consecutive patients with lung cancer, and reverse-transcription polymerase chain reaction (RT-PCR) was used to identify the presence of bacteria and fungi strains.
The analysis of the electrophoresis data pointed out diversity between the samples and the strains that were identified. Mycoplasma strains were identified in all samples. Strains that appeared more often were Staphylococcus epidermidis, Streptococcus mitis and Bacillus strains, followed in descending frequency by Chlamydia, Candida, Listeria, and Haemophilus influenza. In individual patients Legionella pneumophila and Candida tropicalis were detected.
A diversity of pathogens could be identified in surgically extracted tissue samples of patients with lung cancer, with mycoplasma strains being present in all samples. These results point to an etiologic role for chronic infection in lung carcinogenesis. Confirmation of these observations and additional studies are needed to further characterize the etiologic role of inflammation in lung carcinogenesis.
Journal of Cardiothoracic Surgery 10/2011; 6(1):137. DOI:10.1186/1749-8090-6-137 · 1.03 Impact Factor
Nicole Clarke, Jewison Biscocho, Kevin A. Kwei, Jean M. Davidson, Sushmita Sridhar, Xue Gong, Jonathan R. Pollack
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