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BioMed Research International
Volume 2013 (2013), Article ID 158093, 9 pages
Research Article

Release of IL-1β Triggered by Milan Summer PM10: Molecular Pathways Involved in the Cytokine Release

1Polaris Research Centre, Department of Environmental Sciences and Earth Sciences, University of Milano-Bicocca, Piazza della Scienza 1, 20126 Milano, Italy
2Department of Biology and Biotecnology, University of Pavia, Via Ferrata 1, 27100 Pavia, Italy
3Division of Environmental Medicine, Norwegian Institute of Public Health, P.O. Box 4404, Nydalen, 0403 Oslo, Norway
4UTTS Saluggia, ENEA, Strada Crescentino, 13040 Saluggia, Italy

Received 2 October 2012; Revised 22 December 2012; Accepted 3 January 2013

Academic Editor: Per Schwarze

Copyright © 2013 Rossella Bengalli et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Particulate matter (PM) exposure is related to pulmonary and cardiovascular diseases, with increased inflammatory status. The release of the proinflammatory interleukin- (IL-) 1β, is controlled by a dual pathway, the formation of inactive pro-IL-1β, through Toll-like receptors (TLRs) activation, and its cleavage by NLRP3 inflammasome. THP-1-derived macrophages were exposed for 6 h to 2.5 μg/cm2 of Milan PM10, and the potential to promote IL-1β release by binding TLRs and activating NLRP3 has been examined. Summer PM10, induced a marked IL-1β response in the absence of LPS priming (50-fold increase compared to unexposed cells), which was reduced by caspase-1 inhibition (91% of inhibition respect summer PM10-treated cells) and by TLR-2 and TLR-4 inhibitors (66% and 53% of inhibition, resp.). Furthermore, summer PM10 increased the number of early endosomes, and oxidative stress inhibition nearly abolished PM10-induced IL-1β response (90% of inhibition). These findings suggest that summer PM10 contains constituents both related to the activation of membrane TLRs and activation of the inflammasome NLPR3 and that TLRs activation is of pivotal importance for the magnitude of the response. ROS formation seems important for PM10-induced IL-1β response, but further investigations are needed to elucidate the molecular pathway by which this effect is mediated.