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Effects of diesel exhaust particles on macrophage polarization
N Labranche1, C El Khattabi1, G Berkenboom2
11 Laboratory of Physiology and Pharmacology, Faculty of Pharmacy, Université Libre de Bruxelles (ULB), Brussels, Belgium.
Background:
Exposure to diesel exhaust particles (DEP) has long been associated with increased cardiovascular morbidity and mortality. The development of DEP toxicity seems to be linked to inflammation in which macrophages play a critical role. Macrophages can be polarized into proinflammatory M1 or anti-inflammatory M2 macrophages. The aim of this study was to identify the role of inflammation in DEP-induced toxicity by assessing the effects of DEP on macrophage polarization.
Methods:
Monocyte-derived macrophages (Mϕ) were stimulated with interferon γ and lipopolysaccharide or interleukin (IL)-4 to obtain M1 and M2 subtypes, respectively. To test the polarization capacity of DEP, Mϕ cells were exposed to DEP and compared to Mϕ, M1, and M2. We also studied the effects of DEP on already-polarized M1 or M2. The M1 markers assessed were tumor necrosis factor α (TNF-α) and IL-1β, while the M2 markers were the mannose receptor C type 1 (MRC-1) and transglutaminase 2 (TGM2).
Results:
Western blots revealed a 31 kDa band corresponding to pro-IL-1β, but only in M1-polarized macrophages. In M1, we also observed an upregulation of TNF-α messenger RNA (mRNA) expression. MRC-1 and TGM2 mRNA expression were only significantly enhanced in M2. DEP had no effect on any of the M1/M2 markers assessed. Moreover, DEP were not able to modify the phenotype of already-polarized M1 or M2.
Conclusion:
Mϕ incubation with DEP did not have any effect on macrophage polarization, at least on the markers assessed in this study, namely, TNF-α/IL-1β for M1, and MRC-1/TGM2 for M2. Hence, these data argue against an important role of inflammation in DEP-induced vascular toxicity.
Insights
Diesel exhaust particles (DEP) did not alter macrophage polarization markers. These findings suggest inflammation may not play a significant role in DEP-induced vascular toxicity.
Area of Science:
- Immunology
- Environmental Health
- Toxicology
Background:
- Diesel exhaust particles (DEP) are linked to cardiovascular disease.
- Macrophage polarization (M1/M2) is critical in inflammation.
- The role of inflammation in DEP toxicity requires further investigation.
Purpose of the Study:
- To assess the impact of DEP on macrophage polarization.
- To determine if DEP influences M1 or M2 macrophage phenotypes.
Main Methods:
- Differentiated human monocyte-derived macrophages (Mϕ) into M1 and M2 subtypes.
- Exposed Mϕ, M1, and M2 cells to DEP.
- Analyzed M1 markers (TNF-α, IL-1β) and M2 markers (MRC-1, TGM2) via Western blot and mRNA expression.
Main Results:
- M1 macrophages showed increased TNF-α mRNA and pro-IL-1β protein.
- M2 macrophages exhibited enhanced MRC-1 and TGM2 mRNA expression.
- DEP exposure did not affect M1/M2 polarization markers or alter the phenotype of pre-polarized macrophages.
Conclusions:
- Macrophage incubation with DEP did not impact polarization markers (TNF-α/IL-1β for M1, MRC-1/TGM2 for M2).
- These results do not support a significant role for inflammation in DEP-induced vascular toxicity.
