Role of Paris PM(2.5) components in the pro-inflammatory response induced in airway epithelial cells.
Particulate matter (PM) is suspected to play a role in environmentally-induced pathologies. Due to its complex composition, the contribution of each PM components to PM-induced biological effects remains unclear. Four samples of Paris PM(2.5) having different polyaromatic hydrocarbons and metals contents were compared with each other and with their respective aqueous and organic extracts used alone or in combination. The four PM(2.5) samples similarly induced granulocyte macrophage-colony stimulating factor (GM-CSF) release, a pro-inflammatory cytokine, by human bronchial epithelial cells. It results from the activation of upstream signalling pathways and the modulation of the cellular redox state that is different according to PM(2.5) samples. The PM-aqueous extracts contained soluble metals involved in hydroxyl radical production in abiotic conditions. However they slightly contributed to the intracellular reactive oxygen species production and GM-CSF release by comparison with organic extracts. Organic compounds transactivated the xenobiotic responsive element (XRE) and antioxidant responsive element (ARE), leading to increased cytochrome P450 1A1 expression and NADPH-quinone oxydoreductase-1 expression respectively but to different extend according to PM samples underlying differences in their bioavailability. Our study underlines that chemical composition of particles per se is insufficient to predict cellular effects and that the interaction and the bioavailability of the various components were critical.
Baulig
Augustin
A
Univ Paris Diderot-Paris 7, Unit of Functional and Adaptive Biology (BFA) EAC CNRS 7059, Laboratory of Molecular and Cellular Responses to Xenobiotics, 5 rue Thomas Mann, Case 7073, 75205 Paris Cedex 13, France.
Singh
Seema
S
Marchand
Alexandre
A
Schins
Roel
R
Barouki
Robert
R
Garlatti
Michèle
M
Marano
Francelyne
F
Baeza-Squiban
Armelle
A
D001980:Bronchi / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D002460:Cell Line; D019363:Cytochrome P-450 CYP1A1 / Q000235:genetics / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004847:Epithelial Cells / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000378:metabolism*; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism*; D008670:Metals / Q000032:analysis; D016660:NAD(P)H Dehydrogenase (Quinone) / Q000235:genetics / Q000378:metabolism; D010297:Paris; D010316:Particle Size; D052638:Particulate Matter / Q000737:chemistry / Q000633:toxicity*; D011084:Polycyclic Aromatic Hydrocarbons / Q000032:analysis; D012333:RNA, Messenger / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D012621:Seasons; D015398:Signal Transduction / Q000187:drug effects; D013997:Time Factors; D014157:Transcription Factors / Q000378:metabolism; D015533:Transcriptional Activation / Q000187:drug effects; D015854:Up-Regulation
D018836:Inflammation Mediators; D008670:Metals; D052638:Particulate Matter; D011084:Polycyclic Aromatic Hydrocarbons; D012333:RNA, Messenger; D017382:Reactive Oxygen Species; D014157:Transcription Factors; D016178:Granulocyte-Macrophage Colony-Stimulating Factor; D019363:Cytochrome P-450 CYP1A1; D016660:NAD(P)H Dehydrogenase (Quinone); C447479:NQO1 protein, human