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The role of the PM2.5-associated metals in pathogenesis of child Mycoplasma Pneumoniae infections: a systematic review

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Abstract

The peak occurrence of Mycoplasma pneumoniae (M. pneumoniae) infections in childhood and haze episodes is concurrent. Together, the prevalence of macrolide-resistant M. pneumoniae varies among countries might also be related to the concentration of ambient fine particulate mass (aerodynamic diameter ≤2.5 μm, PM2.5). Numerous cohort studies have identified consistent associations between ambient PM2.5 and cardiorespiratory morbidity and mortality. PM2.5 is a carrier of the heavy metals. The relationship between PM2.5-associated metals and M. pneumoniae infections in childhood has been increasingly drawing public attention. First, we reviewed original articles and review papers in Pubmed and Web of Science regarding M. pneumoniae and PM2.5-associated metal and analyzed the structural basis of PM2.5-associated metal interaction with M. pneumoniae. Then, the possible mechanisms of action between them were conjectured. Mechanisms of oxidative stress induction and modulation of the host immune system and inflammatory responses via Toll-like receptors (TLRs) and/or the nuclear factor-kappa B (NF-κB) pathway are postulated to be the result of PM2.5-associated metal complex interaction with M. pneumoniae. In addition, a heavy metal effect on M. pneumoniae-expressed community-acquired respiratory distress syndrome (CARDS) toxin, and activation of the aryl hydrocarbon receptor (AhR) and TLRs to induce the differentiation of T helper (Th) cells are also regarded as important reasons for the influence of the heavy metals on the severity of M. pneumoniae pneumonia and the initial onset and exacerbation of M. pneumoniae associated asthma. PM2.5-associated metals via complex mechanisms can exert a great impact on the host through interaction with M. pneumoniae.

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Acknowledgments

This work was supported by the Project of International Cooperation and Innovation Platform in Guangdong Universities (2013gjhz0007) and the Education Department of Guangdong Government under the Top-tier University Development Scheme for Research and Control of Infectious Diseases (2015038). We would like to thank Dr. Stanley Lin for his constructive comments and English language editing.

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  1. Laboratory of Environmental Medicine and Developmental Toxicology, and Guangdong Provincial Key Laboratory of Infectious Diseases and Molecular Immunopathology, Shantou University Medical College, Shantou, 515041, Guangdong, China

    Wei Hou, Xijin Xu, Junjun Cao & Yu Zhang

  2. People’s Hospital of New District Longhua Shenzhen, Shenzhen, 518109, Guangdong, China

    Wei Hou, Yongge Lei & Liang Chen

  3. Department of Cell Biology and Genetics, Shantou University Medical College, Shantou, 515041, Guangdong, China

    Xijin Xu

  4. Department of Pathology and Medical Biology, University of Groningen, University Medical Center Groningen, Hanzeplein 1, 9713 GZ, Groningen, The Netherlands

    Junjun Cao

  5. School of Environment, Guangzhou Key Laboratory of Environmental Exposure and Health, Guangdong Key Laboratory of Environmental Pollution and Health, Jinan University, Guangzhou, 510632, China

    Xia Huo

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  1. Wei Hou
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Hou, W., Xu, X., Lei, Y. et al. The role of the PM2.5-associated metals in pathogenesis of child Mycoplasma Pneumoniae infections: a systematic review. Environ Sci Pollut Res 23, 10604–10614 (2016). https://doi.org/10.1007/s11356-016-6535-2

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