抑制吞噬作用和溶酶体酸化可抑制神经毒性朊病毒肽诱导的 BV2 小胶质细胞 NALP3 炎性体激活。
Inhibition of phagocytosis and lysosomal acidification suppresses neurotoxic prion peptide-induced NALP3 inflammasome activation in BV2 microglia.
机构信息
Key Lab of Animal Epidemiology and Zoonosis, Ministry of Agriculture, National Animal Transmissible Spongiform Encephalopathy Laboratory, College of Veterinary Medicine, China Agricultural University, Beijing 100193, China.
出版信息
J Neuroimmunol. 2013 Jul 15;260(1-2):121-5. doi: 10.1016/j.jneuroim.2013.04.016. Epub 2013 May 13.
Prion diseases are neurodegenerative disorders characterized by the accumulation of misfolded prion protein. In a previous study, we showed that neurotoxic prion peptide (PrP106-126) induced NALP3 inflammasome activation in mouse primary and immortalized microglia. In the present work, we examined the relevance of phagocytosis and lysosomal acidification to the activation of the NALP3 inflammasome in PrP106-126-stimulated microglia. Our results showed that the inhibition of phagocytosis or lysosomal acidification significantly reduced IL-1β and IL-18 production, downregulated NALP3 and ASC expression, and decreased the expression of proinflammatory factors. We concluded that phagocytosis and lysosomal acidification are necessary for PrP106-126-induced NALP3 activation in BV2 cells.
朊病毒病是一种神经退行性疾病，其特征是错误折叠的朊病毒蛋白积累。在之前的一项研究中，我们表明神经毒性朊病毒肽（PrP106-126）在小鼠原代和永生化小胶质细胞中诱导 NALP3 炎性体激活。在本工作中，我们研究了吞噬作用和溶酶体酸化与 PrP106-126 刺激的小胶质细胞中 NALP3 炎性体激活的相关性。结果表明，吞噬作用或溶酶体酸化的抑制显著降低了 IL-1β 和 IL-18 的产生，下调了 NALP3 和 ASC 的表达，并降低了促炎因子的表达。我们得出结论，吞噬作用和溶酶体酸化是 PrP106-126 诱导 BV2 细胞中 NALP3 激活所必需的。
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