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PM2.5 impairs macrophage functions to exacerbate pneumococcus-induced pulmonary pathogenesis

Authors
  • Chen, Yu-Wen1
  • Huang, Mei-Zi1
  • Chen, Chyi-Liang2
  • Kuo, Chieh-Ying1
  • Yang, Chia-Yu1, 1, 3
  • Chiang-Ni, Chuan1, 2
  • Chen, Yi-Ywan M.1, 2
  • Hsieh, Chia-Ming1
  • Wu, Hui-Yu1
  • Kuo, Ming-Ling1, 2
  • Chiu, Cheng-Hsun1, 2
  • Lai, Chih-Ho1, 2, 4, 5
  • 1 Chang Gung University, Taoyuan, Taiwan , Taoyuan (Taiwan)
  • 2 Chang Gung Memorial Hospital, Linkou, Taiwan , Linkou (Taiwan)
  • 3 Chang Gung Memorial Hospital, Taoyuan, Taiwan , Taoyuan (Taiwan)
  • 4 China Medical University, Taichung, Taiwan , Taichung (Taiwan)
  • 5 Asia University, Taichung, Taiwan , Taichung (Taiwan)
Type
Published Article
Journal
Particle and Fibre Toxicology
Publisher
BioMed Central
Publication Date
Aug 04, 2020
Volume
17
Issue
1
Identifiers
DOI: 10.1186/s12989-020-00362-2
Source
Springer Nature
Keywords
License
Green

Abstract

BackgroundPneumococcus is one of the most common human airway pathogens that causes life-threatening infections. Ambient fine particulate matter (PM) with aerodynamic diameter ≤ 2.5 μm (PM2.5) is known to significantly contribute to respiratory diseases. PM2.5-induced airway inflammation may decrease innate immune defenses against bacterial infection. However, there is currently limited information available regarding the effect of PM2.5 exposure on molecular interactions between pneumococcus and macrophages.ResultsPM2.5 exposure hampered macrophage functions, including phagocytosis and proinflammatory cytokine production, in response to pneumococcal infection. In a PM2.5-exposed pneumococcus-infected mouse model, PM2.5 subverted the pulmonary immune response and caused leukocyte infiltration. Further, PM2.5 exposure suppressed the levels of CXCL10 and its receptor, CXCR3, by inhibiting the PI3K/Akt and MAPK pathways.ConclusionsThe effect of PM2.5 exposure on macrophage activity enhances pneumococcal infectivity and aggravates pulmonary pathogenesis.

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