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Background: This case-control study investigated the role of Chlamydia pneumoniae (Cpn) infection in the pathogenesis of lung cancer and the combined and interaction effect of Cpn infection, smoking, and various environmental factors.
Methods: The study comprised 449 lung cancer patients and 512 age- and gender-matched healthy controls. All participants provided a 5 ml fasting peripheral venous blood sample for testing Cpn-specific IgG and IgA by using micro-immunofluorescence. Besides analyzing the associations between Cpn and lung cancer, combined effect analysis, logistic regression, and the Excel table made by Andersson were used to analyze the combined and interaction effects of Cpn and environmental factors on lung cancer.
Results: Compared to those with no evidence of serum Cpn IgA or Cpn IgG, those with both Cpn IgG+ and IgA+ had 2.00 times the risk (95% CI: 1.34–3.00) of developing lung cancer. Cpn IgG+ or IgA+ was associated with a significantly increased risk of lung cancer among smokers; the adjusted odds ratio (OR) was 1.79 (95% CI: 1.10–2.91) and 2.27 (95% CI: 1.38–3.72), respectively. Those exposed to passive smoking with Cpn IgG+ or IgA+ also showed an increased risk of lung cancer; the adjusted OR was 1.82 (95% CI: 1.20–2.77) or 1.87 (95% CI: 1.22–2.87), respectively. Similar results were also observed among alcohol drinkers. Multiplicative and additive interactions were not observed between Cpn infection and environmental factors. The combined effects of Cpn IgG+ or IgA+ with smoking, passive smoking, and family history of cancer on lung cancer were determined.
Conclusion: Cpn infection is potentially associated with primary lung cancer in the Chinese Han population and has combined effects with smoking, passive smoking, and family history of cancer.
Keywords
Chlamydia pneumoniae infection, case-control study, environmental factors, lung cancer
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CURRENT STATUS: Published
View the published article at BMC Cancer.
Version 2
Posted 07 Aug, 2020
No community comments so far
Editorial decision: Minor revision
On 09 Sep, 2020
Review #1 received
Received 27 Aug, 2020
Review #2 received
Received 15 Aug, 2020
Reviewer #2 agreed
On 12 Aug, 2020
Reviewer #1 agreed
On 10 Aug, 2020
Reviewers invited
Invitations sent on 09 Aug, 2020
Editor assigned
On 30 Jul, 2020
Submission checks complete
On 29 Jul, 2020
Editor invited
On 29 Jul, 2020
No comments provided
Editorial decision: Major revision
On 17 Jun, 2020
Review #3 received
Received 15 Jun, 2020
Reviewer #3 agreed
On 24 May, 2020
Review #2 received
Received 16 May, 2020
Reviewer #2 agreed
On 28 Apr, 2020
Review #1 received
Received 06 Apr, 2020
Reviewer #1 agreed
On 21 Mar, 2020
Reviewers invited
Invitations sent on 23 Feb, 2020
Editor assigned
On 20 Feb, 2020
Submission checks complete
On 18 Feb, 2020
Editor invited
On 17 Feb, 2020
First submitted
On 11 Feb, 2020
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A new preprint design is coming!
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See the published version of this preprint at BMC Cancer.
This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Research article
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Published
View the published article at BMC Cancer.
Version 2
Posted 07 Aug, 2020
No community comments so far
Editorial decision: Minor revision
On 09 Sep, 2020
Review #1 received
Received 27 Aug, 2020
Review #2 received
Received 15 Aug, 2020
Reviewer #2 agreed
On 12 Aug, 2020
Reviewer #1 agreed
On 10 Aug, 2020
Reviewers invited
Invitations sent on 09 Aug, 2020
Editor assigned
On 30 Jul, 2020
Submission checks complete
On 29 Jul, 2020
Editor invited
On 29 Jul, 2020
No comments provided
Editorial decision: Major revision
On 17 Jun, 2020
Review #3 received
Received 15 Jun, 2020
Reviewer #3 agreed
On 24 May, 2020
Review #2 received
Received 16 May, 2020
Reviewer #2 agreed
On 28 Apr, 2020
Review #1 received
Received 06 Apr, 2020
Reviewer #1 agreed
On 21 Mar, 2020
Reviewers invited
Invitations sent on 23 Feb, 2020
Editor assigned
On 20 Feb, 2020
Submission checks complete
On 18 Feb, 2020
Editor invited
On 17 Feb, 2020
First submitted
On 11 Feb, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
License:
This work is licensed under a CC BY 4.0 License. Read Full License
View the published article at BMC Cancer.
Background: This case-control study investigated the role of Chlamydia pneumoniae (Cpn) infection in the pathogenesis of lung cancer and the combined and interaction effect of Cpn infection, smoking, and various environmental factors.
Methods: The study comprised 449 lung cancer patients and 512 age- and gender-matched healthy controls. All participants provided a 5 ml fasting peripheral venous blood sample for testing Cpn-specific IgG and IgA by using micro-immunofluorescence. Besides analyzing the associations between Cpn and lung cancer, combined effect analysis, logistic regression, and the Excel table made by Andersson were used to analyze the combined and interaction effects of Cpn and environmental factors on lung cancer.
Results: Compared to those with no evidence of serum Cpn IgA or Cpn IgG, those with both Cpn IgG+ and IgA+ had 2.00 times the risk (95% CI: 1.34–3.00) of developing lung cancer. Cpn IgG+ or IgA+ was associated with a significantly increased risk of lung cancer among smokers; the adjusted odds ratio (OR) was 1.79 (95% CI: 1.10–2.91) and 2.27 (95% CI: 1.38–3.72), respectively. Those exposed to passive smoking with Cpn IgG+ or IgA+ also showed an increased risk of lung cancer; the adjusted OR was 1.82 (95% CI: 1.20–2.77) or 1.87 (95% CI: 1.22–2.87), respectively. Similar results were also observed among alcohol drinkers. Multiplicative and additive interactions were not observed between Cpn infection and environmental factors. The combined effects of Cpn IgG+ or IgA+ with smoking, passive smoking, and family history of cancer on lung cancer were determined.
Conclusion: Cpn infection is potentially associated with primary lung cancer in the Chinese Han population and has combined effects with smoking, passive smoking, and family history of cancer.
Figure 1
Figure 2
This is a list of supplementary files associated with this preprint. Click to download.
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