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Particulate matter (PM) exposure is related to pulmonary and cardiovascular diseases, with increased inflammatory status. The release of the proinflammatory interleukin- (IL-) 1  β  , is controlled by a dual pathway, the formation of inactive pro-IL-1  β  , through Toll-like receptors (TLRs) activation, and its cleavage by NLRP3 inflammasome. THP-1-derived macrophages were exposed for 6 h to 2.5   μ  g/cm 2  of Milan PM 10 , and the potential to promote IL-1  β   release by binding TLRs and activating NLRP3 has been examined. Summer PM 10 , induced a marked IL-1  β   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 PM 10 -treated cells) and by TLR-2 and TLR-4 inhibitors (66% and 53% of inhibition, resp.). Furthermore, summer PM 10  increased the number of early endosomes, and oxidative stress inhibition nearly abolished PM 10 -induced IL-1  β   response (90% of inhibition). These findings suggest that summer PM 10  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 PM 10 -induced IL-1  β   response, but further investigations are needed to elucidate the molecular pathway by which this effect is mediated.

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

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