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Diesel exhaust particle exposure compromises macrophage mitochondrial physiology
Author(s) -
Gibbs Jonathan,
Dallon Blake,
Lewis Joshua,
Tessem Jeffery S.,
Reynolds Paul R.,
Bikman Benjamin T.
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.470.7
Subject(s) - macrophage , mitochondrion , diesel exhaust , microbiology and biotechnology , alveolar macrophage , function (biology) , chemistry , biology , immunology , diesel fuel , biochemistry , in vitro , organic chemistry
Diesel exhaust particles (DEP) are known pathogenic pollutants. Given the ubiquitous presence of the macrophage throughout the body, including the lungs, as well as their critical role in tissue and organismal homeostasis, we sought to determine the effect of DEP exposure on macrophage mitochondrial function. RAW 264.7 murine macrophages were treated with DEP for 24 hours followed by multiple mitochondrial assays. Not only was mitochondrial content diminished following DEP exposure, but also existing mitochondria produced increased H 2 O 2 and less ATP. Similarly, following repeated DEP exposures in whole mice, pulmonary macrophages were isolated and we found similar mitochondrial consequences. Altogether, these data suggest that DEP exposure may compromise macrophage function via pathologic alterations in macrophage mitochondrial function.