Abstract
Inflammasome activation is gaining recognition as an important mechanism for protection during viral infection. Here, we investigate whether Rift Valley fever virus, a negative-strand RNA virus, can induce inflammasome responses and IL-1β processing in immune cells. We have determined that RVFV induces NLRP3 inflammasome activation in murine dendritic cells, and that this process is dependent upon ASC and caspase-1. Furthermore, absence of the cellular RNA helicase adaptor protein MAVS/IPS-1 significantly reduces extracellular IL-1β during infection. Finally, direct imaging using confocal microscopy shows that the MAVS protein co-localizes with NLRP3 in the cytoplasm of RVFV infected cells.
Keywords:
ASC; Caspase-1; Dendritic cells; IL-1β; Inflammasome; Murine; NLRP3; Rift Valley fever virus; Virus.
© 2013 Published by Elsevier Inc.
Publication types
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Research Support, N.I.H., Extramural
MeSH terms
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Adaptor Proteins, Signal Transducing / genetics
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Adaptor Proteins, Signal Transducing / immunology
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Animals
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Carrier Proteins / genetics
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Carrier Proteins / immunology*
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Caspase 1 / genetics
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Caspase 1 / immunology
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Dendritic Cells / immunology
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Dendritic Cells / virology
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Female
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Humans
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Inflammasomes / genetics
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Inflammasomes / immunology*
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Interleukin-1beta / genetics
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Interleukin-1beta / immunology
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Male
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Mice
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Mice, Inbred C57BL
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Mice, Knockout
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NLR Family, Pyrin Domain-Containing 3 Protein
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Rift Valley Fever / genetics
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Rift Valley Fever / immunology*
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Rift Valley Fever / virology
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Rift Valley fever virus / genetics
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Rift Valley fever virus / physiology*
Substances
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Adaptor Proteins, Signal Transducing
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Carrier Proteins
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IPS-1 protein, mouse
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Inflammasomes
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Interleukin-1beta
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NLR Family, Pyrin Domain-Containing 3 Protein
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Nlrp3 protein, mouse
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Caspase 1