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Impact of caspase-1/11, -3, -7, or IL-1β/IL-18 deficiency on rabies virus-induced macrophage cell death and onset of disease

Elodie Kip UGent, F Nazé, V Suin, Tom Vanden Berghe UGent, A Francart, S Lamoral, Peter Vandenabeele UGent, Rudi Beyaert UGent, Steven Van Gucht UGent and M Kalai (2017) CELL DEATH DISCOVERY. 3.
abstract
Rabies virus is a highly neurovirulent RNA virus, which causes about 59000 deaths in humans each year. Previously, we described macrophage cytotoxicity upon infection with rabies virus. Here we examined the type of cell death and the role of specific caspases in cell death and disease development upon infection with two laboratory strains of rabies virus: Challenge Virus Standard strain-11 (CVS-11) is highly neurotropic and lethal for mice, while the attenuated Evelyn-Rotnycki-Abelseth (ERA) strain has a broader cell tropism, is non-lethal and has been used as an oral vaccine for animals. Infection of Mf4/4 macrophages with both strains led to caspase-1 activation and IL-1β and IL-18 production, as well as activation of caspases-3, -7, -8, and -9. Moreover, absence of caspase-3, but not of caspase-1 and -11 or -7, partially inhibited virus-induced cell death of bone marrow-derived macrophages. Intranasal inoculation with CVS-11 of mice deficient for either caspase-1 and -11 or -7 or both IL-1β and IL-18 led to general brain infection and lethal disease similar to wild-type mice. Deficiency of caspase-3, on the other hand, significantly delayed the onset of disease, but did not prevent final lethal outcome. Interestingly, deficiency of caspase-1/11, the key executioner of pyroptosis, aggravated disease severity caused by ERA virus, whereas wild-type mice or mice deficient for either caspase-3, -7, or both IL-1β and IL-18 presented the typical mild symptoms associated with ERA virus. In conclusion, rabies virus infection of macrophages induces caspase-1- and caspase-3-dependent cell death. In vivo caspase-1/11 and caspase-3 differently affect disease development in response to infection with the attenuated ERA strain or the virulent CVS-11 strain, respectively. Inflammatory caspases seem to control attenuated rabies virus infection, while caspase-3 aggravates virulent rabies virus infection.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
journal title
CELL DEATH DISCOVERY
Cell Death Discovery
volume
3
article number
17012
pages
10 pages
ISSN
2058-7716
DOI
10.1038/cddiscovery.2017.12
language
English
UGent publication?
yes
classification
A2
additional info
the first two authors contributed equally to this work; the last three authors share senior authorship
copyright statement
Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
id
8555803
handle
http://hdl.handle.net/1854/LU-8555803
date created
2018-03-15 10:06:29
date last changed
2018-05-29 07:51:31
@article{8555803,
  abstract     = {Rabies virus is a highly neurovirulent RNA virus, which causes about 59000 deaths in humans each year. Previously, we described macrophage cytotoxicity upon infection with rabies virus. Here we examined the type of cell death and the role of specific caspases in cell death and disease development upon infection with two laboratory strains of rabies virus: Challenge Virus Standard strain-11 (CVS-11) is highly neurotropic and lethal for mice, while the attenuated Evelyn-Rotnycki-Abelseth (ERA) strain has a broader cell tropism, is non-lethal and has been used as an oral vaccine for animals. Infection of Mf4/4 macrophages with both strains led to caspase-1 activation and IL-1\ensuremath{\beta} and IL-18 production, as well as activation of caspases-3, -7, -8, and -9. Moreover, absence of caspase-3, but not of caspase-1 and -11 or -7, partially inhibited virus-induced cell death of bone marrow-derived macrophages. Intranasal inoculation with CVS-11 of mice deficient for either caspase-1 and -11 or -7 or both IL-1\ensuremath{\beta} and IL-18 led to general brain infection and lethal disease similar to wild-type mice. Deficiency of caspase-3, on the other hand, significantly delayed the onset of disease, but did not prevent final lethal outcome. Interestingly, deficiency of caspase-1/11, the key executioner of pyroptosis, aggravated disease severity caused by ERA virus, whereas wild-type mice or mice deficient for either caspase-3, -7, or both IL-1\ensuremath{\beta} and IL-18 presented the typical mild symptoms associated with ERA virus. In conclusion, rabies virus infection of macrophages induces caspase-1- and caspase-3-dependent cell death. In vivo caspase-1/11 and caspase-3 differently affect disease development in response to infection with the attenuated ERA strain or the virulent CVS-11 strain, respectively. Inflammatory caspases seem to control attenuated rabies virus infection, while caspase-3 aggravates virulent rabies virus infection.},
  articleno    = {17012},
  author       = {Kip, Elodie and Naz{\'e}, F and Suin, V and Vanden Berghe, Tom and Francart, A and Lamoral, S and Vandenabeele, Peter and Beyaert, Rudi and Van Gucht, Steven and Kalai, M},
  issn         = {2058-7716},
  journal      = {CELL DEATH DISCOVERY},
  language     = {eng},
  pages        = {10},
  title        = {Impact of caspase-1/11, -3, -7, or IL-1\ensuremath{\beta}/IL-18 deficiency on rabies virus-induced macrophage cell death and onset of disease},
  url          = {http://dx.doi.org/10.1038/cddiscovery.2017.12},
  volume       = {3},
  year         = {2017},
}

Chicago
Kip, Elodie, F Nazé, V Suin, Tom Vanden Berghe, A Francart, S Lamoral, Peter Vandenabeele, Rudi Beyaert, Steven Van Gucht, and M Kalai. 2017. “Impact of Caspase-1/11, -3, -7, or IL-1β/IL-18 Deficiency on Rabies Virus-induced Macrophage Cell Death and Onset of Disease.” Cell Death Discovery 3.
APA
Kip, E., Nazé, F., Suin, V., Vanden Berghe, T., Francart, A., Lamoral, S., Vandenabeele, P., et al. (2017). Impact of caspase-1/11, -3, -7, or IL-1β/IL-18 deficiency on rabies virus-induced macrophage cell death and onset of disease. CELL DEATH DISCOVERY, 3.
Vancouver
1.
Kip E, Nazé F, Suin V, Vanden Berghe T, Francart A, Lamoral S, et al. Impact of caspase-1/11, -3, -7, or IL-1β/IL-18 deficiency on rabies virus-induced macrophage cell death and onset of disease. CELL DEATH DISCOVERY. 2017;3.
MLA
Kip, Elodie, F Nazé, V Suin, et al. “Impact of Caspase-1/11, -3, -7, or IL-1β/IL-18 Deficiency on Rabies Virus-induced Macrophage Cell Death and Onset of Disease.” CELL DEATH DISCOVERY 3 (2017): n. pag. Print.