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Chlamydia pneumoniae and chronic asthma: Updated systematic review and meta-analysis of population attributable risk

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  • David L Hahn

Abstract

Background: Chlamydia pneumoniae (Cp) is an obligate intracellular human respiratory pathogen producing persisting lung infection with a plausible link to asthma pathogenesis. The population attributable risk of potentially treatable Cp infection in asthma has not been reported. Methods: The author searched from 2000 to 2020 inclusive for previously un-reviewed and new cross sectional and prospective controlled studies of Cp biomarkers and chronic asthma in both children and adults. Qualitative descriptive results and quantitative estimates of population attributable risk for selected biomarkers (specific IgG, IgA and IgE) are presented. Findings: No large, long-term prospective population-based studies of Cp infection and asthma were identified. About half of case-control studies reported one or more significant associations of Cp biomarkers and chronic asthma. Heterogeneity of results by age group (pediatric v adult asthma), severity category (severe/uncontrolled, moderate/partly controlled, mild/controlled) and antibody isotype (specific IgG, IgA, IgE) were suggested by the qualitative results and confirmed by meta-analyses. The population attributable risks for Cp-specific IgG and IgA were nul in children and were 6% (95% confidence interval 2%-10%, p = 0.002) and 13% (9%-18%, p

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  • David L Hahn, 2021. "Chlamydia pneumoniae and chronic asthma: Updated systematic review and meta-analysis of population attributable risk," PLOS ONE, Public Library of Science, vol. 16(4), pages 1-21, April.
    • Handle: RePEc:plo:pone00:0250034
    DOI: 10.1371/journal.pone.0250034
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    Cited by:

    1. Fabienne Kocher & Violetta Applegate & Jens Reiners & Astrid Port & Dominik Spona & Sebastian Hänsch & Amin Mirzaiebadizi & Mohammad Reza Ahmadian & Sander H. J. Smits & Johannes H. Hegemann & Katja M, 2024. "The Chlamydia pneumoniae effector SemD exploits its host’s endocytic machinery by structural and functional mimicry," Nature Communications, Nature, vol. 15(1), pages 1-16, December.

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