Reduced alveolar macrophage migration induced by acute ambient particle (PM10) exposure
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Increased levels of particulate air pollution (PM10) have been implicated as a causal agent in pulmonary disease exacerbation and increased deaths from respiratory and cardiovascular disorders. The exact mechanism by which PM10 drives toxicity in the lung is still unknown, but studies have focused on inhibition of macrophage function and impaired alveolar clearance mechanisms. To assess the effects of PM10 on pulmonary macrophage clearance mechanisms ex vivo, Wistar rats were instilled with 125 or 250 μg of PM10 collected from the North Kensington, London. Control rats were instilled with sterile saline. The rats were sacrificed after 18 h and a bronchoalveolar lavage (BAL) was performed. Macrophages isolated from the BAL fluid were assessed for ability to migrate towards a positive chemoattractant (ZAS) ex vivo and to perform phagocytosis. Macrophages isolated from the PM10-exposed rats showed inhibition of potential to migrate. Macrophage phagocytic ability ex vivo was also significantly reduced by the presence of PM10 inside the cells. This study indicates that acute PM10 exposure diminishes macrophage motility and phagocytosis in a manner that could prove deleterious to particle clearance from the alveolar region of the lung. Decreased particle clearance promotes inflammation, and hence, warrants further investigation in relation to the effects of chronic PM10 exposure on macrophage clearance mechanisms and establishing the mechanisms behind decreased macrophage migration.
KeywordsAir pollution Macrophages Lung Phagocytosis Chemotaxis PM10
bovine serum albumin
complement protein C5a
concentrated ambient particles
enzyme-linked immunosorbent assay
macrophage inflammatory protein 2
nicotinamide adenine dinucleotide (reduced)
particulate air pollution with a diameter ≤ 10 μm
streptavidin–horse radish peroxidase
tumour necrosis factor alpha
The authors would like to acknowledge Napier University, Edinburgh for the funding of this project. PGB would like to acknowledge the experimental assistance of Dr. Gary Hutchison.
Conflict of Interest Statement
None of the authors of this manuscript have any conflicts of interest to declare.
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