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lüll Activation of NLRP3 inflammasome in alveolar macrophages contributes to mechanical stretch-induced lung inflammation and injury Wu J; Yan Z; Schwartz DE; Yu J; Malik AB; Hu GJ Immunol 2013[Apr]; 190 (7): 3590-9Mechanical ventilation of lungs is capable of activating the innate immune system and inducing sterile inflammatory response. The proinflammatory cytokine IL-1beta is among the definitive markers for accurately identifying ventilator-induced lung inflammation. However, mechanisms of IL-1beta release during mechanical ventilation are unknown. In this study, we show that cyclic stretch activates the nucleotide-binding oligomerization domain-like receptor containing pyrin domain 3 (NLRP3) inflammasomes and induces the release of IL-1beta in mouse alveolar macrophages via caspase-1- and TLR4-dependent mechanisms. We also observed that NADPH oxidase subunit gp91(phox) was dispensable for stretch-induced cytokine production, whereas mitochondrial generation of reactive oxygen species was required for stretch-induced NLRP3 inflammasome activation and IL-1beta release. Further, mechanical ventilation activated the NLRP3 inflammasomes in mouse alveolar macrophages and increased the production of IL-1beta in vivo. IL-1beta neutralization significantly reduced mechanical ventilation-induced inflammatory lung injury. These findings suggest that the alveolar macrophage NLRP3 inflammasome may sense lung alveolar stretch to induce the release of IL-1beta and hence may contribute to the mechanism of lung inflammatory injury during mechanical ventilation.|Animals[MESH]|Carrier Proteins/*metabolism[MESH]|Caspase 1/metabolism[MESH]|Disease Models, Animal[MESH]|Inflammasomes/*metabolism[MESH]|Interleukin-18/metabolism[MESH]|Interleukin-1beta/metabolism[MESH]|Macrophages, Alveolar/immunology/*metabolism[MESH]|Male[MESH]|Mice[MESH]|Mice, Knockout[MESH]|Mitochondria/metabolism[MESH]|NLR Family, Pyrin Domain-Containing 3 Protein[MESH]|Pneumonia/*etiology/immunology/metabolism[MESH]|Reactive Oxygen Species/metabolism[MESH]|Signal Transduction[MESH]|Toll-Like Receptor 4/metabolism[MESH]|Uric Acid/metabolism[MESH]|Ventilator-Induced Lung Injury/immunology/metabolism[MESH] |