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Diesel Exhaust Particles and the Induction of Macrophage Activation and Dysfunction

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Abstract

Diesel exhaust particles (DEP) are an important component of air particulate matter, generated from the incomplete combustion of fossil fuel in diesel engines. Several epidemiological and experimental data have shown the ability of DEP to induce oxidative stress and pro-inflammatory response as mechanisms in macrophage activation and dysfunction. Macrophages are very important to immunity and immune response due to their ability to phagocyte microbes and parasites. They also respond to toxic chemicals, such as DEP, in the environment and studies have shown that their functions may be impaired by their exposure to DEP. For instance, the ultrafine particles (UFP) of DEP are capable of penetrating deep into the lungs and getting deposited in the alveolar component, where they can mitigate against the phagocytosis function of the alveolar macrophages. In this review, data linking DEP exposure to macrophage activation and dysfunction are addressed together with the various mechanisms involved in these DEP-induced effects.

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Abbreviations

DE:

Diesel exhaust

PM:

Particulate matter

PAH:

Polycyclic aromatic hydrocarbon

CXCL:

Chemokine ligand

IL:

Interleukin

TNFα:

Tumor necrotic factor alpha

NF-kβ:

Nuclear factor kappa B

AP-1:

Activator protein 1

Nrf2:

Nuclear factor (erythroid-derived 2)-like 2-related factor

AhR:

Aryl hydrocarbon receptor

PGE2 :

Prostaglandin E2

AM:

Alveolar macrophages

LPS:

Lipopolysaccharides

GSH:

Reduced glutathione

GSSG:

Oxidized glutathione

NADH:

Reduced nicotinamide adenine dinucleotide

IgE:

Immunoglobulin E

DEP:

Diesel exhaust particle

SRM:

Standard reference material

HUVEC:

Human umbilical vein endothelial cells

MDMs:

Monocyte-derived macrophages

MCP-1:

Monocyte chemotactic protein 1

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Acknowledgements

AOL is a senior lecturer at FUTA, Nigeria.

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Lawal, A.O. Diesel Exhaust Particles and the Induction of Macrophage Activation and Dysfunction. Inflammation 41, 356–363 (2018). https://doi.org/10.1007/s10753-017-0682-6

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