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  • Title: Ventilator-induced lung injury is alleviated by inhibiting NLRP3 inflammasome activation.
    Author: Liu H, Gu C, Liu M, Liu G, Wang D, Liu X, Wang Y.
    Journal: Mol Immunol; 2019 Jul; 111():1-10. PubMed ID: 30952009.
    Abstract:
    BACKGROUND: Mechanical ventilation (MV) is frequently used but can aggravate or cause lung injury, known as ventilator-induced lung injury (VILI). However, the mechanisms are unclear. The NLR family pyrin domain containing 3 (NLRP3) inflammasome is a vital component of innate immunity and is closely related to VILI. METHODS: Mouse lung epithelial (MLE-12) cells were transfected with NLRP3 small interfering RNA (siRNA) or scramble siRNA (sc siRNA) and subjected to 20% cyclic stretch (CS). Wild-type C57BL/6 mice were injected with a liquid complex of NLRP3 siRNA/sc siRNA-Lipofectamine 2000 through the fundus venous plexus before mechanical ventilation. Western blots, immunoprecipitation, ELISAs, flow cytometry, immunofluorescence, and hematoxylin-eosin staining were used to assess the effects of the NLRP3 inflammasome on VILI and the mechanisms of those effects. RESULTS: CS activated the NLRP3 inflammasome by activating NIMA-related kinase 7 (NEK7). NLRP3 depletion inhibited NLRP3 inflammasome activation; alleviated the degradation of cell junction proteins, including p120-catenin (p120) and occludin; ameliorated the colocalization of p120 and E-cadherin; and mitigated the decrease in mitochondrial membrane potential caused by mechanical stretch. Furthermore, after NLRP3 depletion, VILI was attenuated by decreasing IL-1β secretion and pulmonary edema. CONCLUSIONS: Inhibiting NLRP3 inflammasome activation ameliorated VILI, suggesting a potential therapeutic target for the clinical treatment of VILI.
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