Cell Biology and Toxicology

, 24:243

Reduced alveolar macrophage migration induced by acute ambient particle (PM10) exposure

  • Peter G. Barlow
  • David M. Brown
  • Ken Donaldson
  • Janis MacCallum
  • Vicki Stone
Article

DOI: 10.1007/s10565-007-9033-y

Cite this article as:
Barlow, P.G., Brown, D.M., Donaldson, K. et al. Cell Biol Toxicol (2008) 24: 243. doi:10.1007/s10565-007-9033-y

Abstract

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.

Keywords

Air pollutionMacrophagesLungPhagocytosisChemotaxisPM10

Abbreviations

BAL

bronchoalveolar lavage

BSA

bovine serum albumin

C5a

complement protein C5a

CAPS

concentrated ambient particles

ELISA

enzyme-linked immunosorbent assay

GSH

glutathione

HCl

hydrochloric acid

LDH

lactate dehydrogenase

MCE

mucociliary escalator

MIP-2

macrophage inflammatory protein 2

NADH

nicotinamide adenine dinucleotide (reduced)

PBS

phosphate-buffered saline

PM

particulate matter

PM10

particulate air pollution with a diameter ≤ 10 μm

S-HRP

streptavidin–horse radish peroxidase

TiO2

titanium dioxide

TMB

tetramethylbenzidine

TNFα

tumour necrosis factor alpha

ZAS

zymosan-activated serum

Copyright information

© Springer Science+Business Media B.V. 2007

Authors and Affiliations

  • Peter G. Barlow
    • 1
    • 2
  • David M. Brown
    • 2
  • Ken Donaldson
    • 3
  • Janis MacCallum
    • 2
  • Vicki Stone
    • 2
  1. 1.Lung Inflammation Research Group, MRC/University of Edinburgh Centre for Inflammation ResearchQueens Medical Research InstituteEdinburghUK
  2. 2.Biomedicine Research GroupNapier UniversityEdinburghUK
  3. 3.ELEGI/Colt Laboratories, MRC/University of Edinburgh Centre for Inflammation ResearchQueens Medical Research InstituteEdinburghUK