Chlamydia pneumoniae Infection and Risk for Lung Cancer

Infections and Immunoepidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Rockville, MD 20852, USA.
Cancer Epidemiology Biomarkers & Prevention (Impact Factor: 4.13). 06/2010; 19(6):1498-505. DOI: 10.1158/1055-9965.EPI-09-1261
Source: PubMed


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.

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    • "There is evidence for an association between infections with Salmonella typhi and cancer of the hepatic system [9]. Other infections with bacteria such as Citrobacter rodentium in mice [10], Chlamydia pneumonia [11] and Streptococcus bovis [12] 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]. "
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    • "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 [63] [64]. Moreover, a significant association has been found with elevated Chlamydia Hsp-60 seropositivity, thus supporting an etiologic role of C. pneumoniae in lung carcinogenesis [62] [65]. 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 [66]. "
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    • "Indeed, mycoplasma is one of the most often observed pathogen in lung carcinomas [9], and it has been postulated that mycoplasma-infected cells have a higher ability to metastasize in vivo than non-mycoplasma-infected cells [10]. 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]. "
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