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Release of IL-1 β triggered by milan Summer PM10: Molecular pathways involved in the cytokine release

TitleRelease of IL-1 β triggered by milan Summer PM10: Molecular pathways involved in the cytokine release
Publication TypeArticolo su Rivista peer-reviewed
Year of Publication2013
AuthorsBengalli, R., Molteni E., Longhin E., Refsnes M., Camatini M., and Gualtieri Maurizio
JournalBioMed Research International
Volume2013
ISSN23146133
Keywordsair pollutant, Air Pollutants, article, Caspase 1, caspase inhibitor, Caspase Inhibitors, Cell Line, chemistry, controlled study, cryopyrin, Culture media, culture medium, cytokine release, cytology, drug antagonism, drug effect, endocytosis, endosome, Endosomes, Enzyme inhibition, human, human cell, Humans, inflammasome, inflammation, interleukin 1beta, interleukin 1beta converting enzyme, Interleukin-1beta, Italy, lipopolysaccharide, Lipopolysaccharides, macrophage, Macrophages, metabolism, monocyte, Monocytes, Oxidative stress, particulate matter, reactive oxygen metabolite, Reactive Oxygen Species, season, Seasons, summer, TLR2 protein, TLR4 protein, toll like receptor, toll like receptor 2, toll like receptor 4, Toll-Like Receptor 2, Toll-Like Receptor 4
Abstract

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 PM 10-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. © 2013 Rossella Bengalli et al.

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URLhttps://www.scopus.com/inward/record.uri?eid=2-s2.0-84874603412&doi=10.1155%2f2013%2f158093&partnerID=40&md5=3719223590d3c7c7b431aebe8e864ed8
DOI10.1155/2013/158093
Citation KeyBengalli2013