https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:14651 Sat 24 Mar 2018 08:20:46 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:16915 10) activates the nucleotide-binding domain, leucine-rich repeat protein (NLRP) 3 inflammasome in human airway epithelial cells. Our objective was to determine the innate and adaptive immune responses mediated by the airway epithelium NLRP3 inflammasome in response to PM₁₀ exposure. Using in vitro cultures of human airway epithelial cells and in vivo studies with wild-type and Nlrp3^-/- mice, we investigated the downstream consequences of PM₁₀-induced NLPR3 inflammasome activation on cytokine production, cellular inflammation, dendritic cell activation, and PM₁₀-facilitated allergic sensitization. PM₁₀ activates an NLRP3 inflammasome/IL-1 receptor I (IL-1RI) axis in airway epithelial cells, resulting in IL-1β, CC chemokine ligand-20, and granulocyte/macrophage colony–stimulating factor production, which is associated with dendritic cell activation and lung neutrophilia. Despite these profound innate immune responses in the airway epithelium, the NLRP3 inflammasome/IL-1RI axis is dispensable for PM₁₀-facilitated allergic sensitization. We demonstrate the importance of the lung NLRP3 inflammasome in mediating PM₁₀ exposure–associated innate, but not adaptive, immune responses. Our study highlights a mechanism by which PM₁₀ exposure can contribute to the exacerbation of airway disease, but not PM₁₀-facilitated allergic sensitization.]]> Sat 24 Mar 2018 07:58:45 AEDT ]]>