Environmental Science and Pollution Research

, Volume 23, Issue 11, pp 10604–10614 | Cite as

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

  • Wei Hou
  • Xijin Xu
  • Yongge Lei
  • Junjun Cao
  • Yu Zhang
  • Liang Chen
  • Xia Huo
Review Article


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.


M. pneumoniae Childhood PM2.5-associated-metal Oxidative stress TLR NF-κB CARDS toxin AhR 



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.

Compliance with ethical standards

Ethics statement

This manuscript is a review article and does not involve a research protocol requiring approval by the relevant institutional review board or ethics committee.

Conflict of interest

The authors declare that they have no conflict of interest.


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Copyright information

© Springer-Verlag Berlin Heidelberg 2016

Authors and Affiliations

  • Wei Hou
    • 1
    • 2
  • Xijin Xu
    • 1
    • 3
  • Yongge Lei
    • 2
  • Junjun Cao
    • 1
    • 4
  • Yu Zhang
    • 1
  • Liang Chen
    • 2
  • Xia Huo
    • 5
  1. 1.Laboratory of Environmental Medicine and Developmental Toxicology, and Guangdong Provincial Key Laboratory of Infectious Diseases and Molecular ImmunopathologyShantou University Medical CollegeShantouChina
  2. 2.People’s Hospital of New District Longhua ShenzhenShenzhenChina
  3. 3.Department of Cell Biology and GeneticsShantou University Medical CollegeShantouChina
  4. 4.Department of Pathology and Medical BiologyUniversity of Groningen, University Medical Center GroningenGroningenThe Netherlands
  5. 5.School of Environment, Guangzhou Key Laboratory of Environmental Exposure and Health, Guangdong Key Laboratory of Environmental Pollution and HealthJinan UniversityGuangzhouChina

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