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Diesel exhaust particulate matter induces multinucleate cells and zinc transporter-dependent apoptosis in human airway cells

journal contribution
posted on 2007-11-01, 00:00 authored by Leigh AcklandLeigh Ackland, L Zou, David Freestone, S van de Waasenburg, Agnes MichalczykAgnes Michalczyk
The cellular effects of biodiesel emissions particulate matter (BDEP) and petroleum diesel emissions particulate matter (PDEP) were compared using a human airway cell line, A549. At concentrations of 25 µg/ml, diesel particulate matter induced the formation of multinucleate cells. In cells treated with a mixture of 80% PDEP:20% BDEP, 52% of cells were multinucleate cells compared with only 16% of cells treated with 20% PDEP:80% BDEP with a background multinucleate rate of 7%. These results demonstrate a causal relation between the formation of multinucleate cells and exposure to exhaust particulate matter, in particular diesel exhaust. Exposure of A549 cells to PDEP induced apoptosis, seen by active caspase-3 expression and the presence of cleaved pancytokeratin. PDEP exhaust was a much stronger inducer of cellular death through apoptosis than BDEP. There was an eightfold increase in the expression of SLC30A3 (zinc transporter-3 or ZnT3) in cells exposed to 80% PDEP:20% BDEP compared to untreated cells. The increase in ZnT3 expression seen in apoptotic cells following PDEP suggests a role for this zinc transporter in the apoptotic pathway, possibly through controlling zinc fluxes. As exposure to diesel exhaust particles is associated with asthma and apoptosis in airway cells, diesel exhaust particles may directly contribute to asthma by inducing epithelial cell death through apoptotic pathway.

History

Journal

Immunology and cell biology

Volume

85

Issue

8

Pagination

617 - 622

Publisher

Nature Publishing Group

Location

London, England

ISSN

0818-9641

eISSN

1440-1711

Language

eng

Publication classification

C1 Refereed article in a scholarly journal

Copyright notice

2007, Australasian Society for Immunology Inc.