Rift Valley fever virus infection induces activation of the NLRP3 inflammasome

Megan E. Ermler; Zachary Traylor; Krupen Patel; Stefan A. Schattgen; Sivapriya K. Vanaja; Katherine A. Fitzgerald; Amy G. Hise

doi:10.1016/j.virol.2013.11.015

Rift Valley fever virus infection induces activation of the NLRP3 inflammasome

Megan E. Ermler
, Zachary Traylor
, Krupen Patel
, Stefan A. Schattgen
, Sivapriya K. Vanaja
, Katherine A. Fitzgerald
, Amy G. Hise

Research output: Contribution to journal › Article › peer-review

45 Scopus citations

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.

Original language	English
Pages (from-to)	174-180
Number of pages	7
Journal	Virology
Volume	449
DOIs	https://doi.org/10.1016/j.virol.2013.11.015
State	Published - 20 Jan 2014
Externally published	Yes

Keywords

ASC
Caspase-1
Dendritic cells
IL-1β
Inflammasome
Murine
NLRP3
Rift Valley fever virus
Virus

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10.1016/j.virol.2013.11.015

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@article{da85b24a61744b988b629041e8c0dec4,

title = "Rift Valley fever virus infection induces activation of the NLRP3 inflammasome",

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",

author = "Ermler, \{Megan E.\} and Zachary Traylor and Krupen Patel and Schattgen, \{Stefan A.\} and Vanaja, \{Sivapriya K.\} and Fitzgerald, \{Katherine A.\} and Hise, \{Amy G.\}",

note = "Funding Information: We thank Michael Gale, Jr. ( University of Washington, Seattle, Washington ) for providing us with the Rig-I −/− mice, Marco Colonna (Washington University, St. Louis, MO) for the Mda5 −/− mice, Zhijian Chen (UT Southwestern, Dallas, TX) for the Mavs −/− mice, and Richard Flavell (Yale, New Haven, CT) for the Casp-1 −/− mice. We also thank Shinji Makino and Tetsuro Ikegami (University of Texas Medical Branch, Galveston, TX) for providing the attenuated RVFV strains. This work was supported by NIH grant R21AI083693 (A.G.H.) , R21AI079617 (A.G.H) , U54AI057160 to the Midwest Regional Center of Excellence for Biodefense and Emerging Infectious Disease Research (A.G.H). S.V.K was supported by U54AI057159 to the New England Regional Center of Excellence for Biodefense and Emerging Infectious Disease Research. M.E.E was supported in part by NIH Training grant T32AI089474 .",

year = "2014",

month = jan,

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doi = "10.1016/j.virol.2013.11.015",

language = "English",

volume = "449",

pages = "174--180",

journal = "Virology",

issn = "0042-6822",

publisher = "Academic Press Inc.",

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T1 - Rift Valley fever virus infection induces activation of the NLRP3 inflammasome

AU - Ermler, Megan E.

AU - Traylor, Zachary

AU - Patel, Krupen

AU - Schattgen, Stefan A.

AU - Vanaja, Sivapriya K.

AU - Fitzgerald, Katherine A.

AU - Hise, Amy G.

N1 - Funding Information: We thank Michael Gale, Jr. ( University of Washington, Seattle, Washington ) for providing us with the Rig-I −/− mice, Marco Colonna (Washington University, St. Louis, MO) for the Mda5 −/− mice, Zhijian Chen (UT Southwestern, Dallas, TX) for the Mavs −/− mice, and Richard Flavell (Yale, New Haven, CT) for the Casp-1 −/− mice. We also thank Shinji Makino and Tetsuro Ikegami (University of Texas Medical Branch, Galveston, TX) for providing the attenuated RVFV strains. This work was supported by NIH grant R21AI083693 (A.G.H.) , R21AI079617 (A.G.H) , U54AI057160 to the Midwest Regional Center of Excellence for Biodefense and Emerging Infectious Disease Research (A.G.H). S.V.K was supported by U54AI057159 to the New England Regional Center of Excellence for Biodefense and Emerging Infectious Disease Research. M.E.E was supported in part by NIH Training grant T32AI089474 .

PY - 2014/1/20

Y1 - 2014/1/20

N2 - 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.

AB - 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.

KW - ASC

KW - Caspase-1

KW - Dendritic cells

KW - IL-1β

KW - Inflammasome

KW - Murine

KW - NLRP3

KW - Rift Valley fever virus

KW - Virus

UR - https://www.scopus.com/pages/publications/84896983616

U2 - 10.1016/j.virol.2013.11.015

DO - 10.1016/j.virol.2013.11.015

M3 - Article

C2 - 24418550

AN - SCOPUS:84896983616

SN - 0042-6822

VL - 449

SP - 174

EP - 180

JO - Virology

JF - Virology

ER -

Rift Valley fever virus infection induces activation of the NLRP3 inflammasome

Abstract

Keywords

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