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Inhibition of phagocytosis and lysosomal acidification suppresses neurotoxic prion peptide-induced NALP3 inflammasome activation in BV2 microglia.

Abstract：

: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.

journal_name

J Neuroimmunol

journal_title

Journal of neuroimmunology

authors

Shi F,Yang Y,Kouadir M,Fu Y,Yang L,Zhou X,Yin X,Zhao D

doi

10.1016/j.jneuroim.2013.04.016

subject

Has Abstract

pub_date

2013-07-15 00:00:00

pages

121-5

issue

1-2

eissn

0165-5728

issn

1872-8421

pii

S0165-5728(13)00100-8

journal_volume

260

pub_type

杂志文章

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