Abstract：
:Activation of the NLRP3 inflammasome and subsequent maturation of IL-1β have been implicated in acute lung injury (ALI), resulting in inflammation and fibrosis. We investigated the role of vimentin, a type III intermediate filament, in this process using three well-characterized murine models of ALI known to require NLRP3 inflammasome activation. We demonstrate that central pathophysiologic events in ALI (inflammation, IL-1β levels, endothelial and alveolar epithelial barrier permeability, remodelling and fibrosis) are attenuated in the lungs of Vim(-/-) mice challenged with LPS, bleomycin and asbestos. Bone marrow chimeric mice lacking vimentin have reduced IL-1β levels and attenuated lung injury and fibrosis following bleomycin exposure. Furthermore, decreased active caspase-1 and IL-1β levels are observed in vitro in Vim(-/-) and vimentin-knockdown macrophages. Importantly, we show direct protein-protein interaction between NLRP3 and vimentin. This study provides insights into lung inflammation and fibrosis and suggests that vimentin may be a key regulator of the NLRP3 inflammasome.
journal_name
Nat Communjournal_title
Nature communicationsauthors
dos Santos G,Rogel MR,Baker MA,Troken JR,Urich D,Morales-Nebreda L,Sennello JA,Kutuzov MA,Sitikov A,Davis JM,Lam AP,Cheresh P,Kamp D,Shumaker DK,Budinger GR,Ridge KMdoi
10.1038/ncomms7574subject
Has Abstractpub_date
2015-03-12 00:00:00pages
6574issn
2041-1723pii
ncomms7574journal_volume
6pub_type
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