Premium
Oxidative and Inflammatory Responses of Monocytes or Macrophages to Ambient Particulate Matter
Author(s) -
Bliss Bishop Charles,
Solaimani Parissa,
Campbell Arezoo
Publication year - 2016
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.30.1_supplement.lb502
Subject(s) - oxidative stress , particulates , inflammation , reactive oxygen species , monocyte , oxidative phosphorylation , macrophage , chemistry , immunology , immune system , inflammatory response , biology , biochemistry , in vitro , organic chemistry
Oxidative stress and inflammation are two major responses to ambient particulate matter (PM) and are thought to be responsible for the majority of its adverse health impacts. The hypothesis of this study is that monocytes and macrophages will have different responses to PM and that the oxidative and inflammatory responses will be linked. A human monocytic cell line (THP‐1) was used as a model for monocytes. These cells were also differentiated to macrophages via exposure to phorbol ester (PMA) for 48 hours. These cells were then exposed to three different size fractions of particulate matter: PM 10 (coarse), PM 2.5 (fine), and PM 0.1 (ultrafine) for 24 hours. Oxidative stress was measured using the DCFH‐DA assay. Reactive oxygen species (ROS) increased compared to the control, but the increase was not dependent on PM size. There was no significant difference in ROS levels in monocytes compared to macrophages. Inflammatory cytokines TNF‐α and IL‐1β were measured using ELISA. In both monocytes and macrophages, fine and coarse particles elicited a significant increase. No significance occurred after exposure to ultrafine particles and there was no difference in the response to monocytes compared to macrophages. This study suggests that monocytes and macrophages respond similarly to particulate matter. Also, PM‐induced oxidative and inflammatory responses may not be directly linked. The mechanism by which PM causes these observed responses in immune competent cells is the subject of future studies in the laboratory. Support or Funding Information British Petroleum/ Southern California Air Quality Management District (BP/SCAQMD Award #11527) and Western University of Health Sciences