2015
DOI: 10.1073/pnas.1419090112
|View full text |Cite
|
Sign up to set email alerts
|

AIM2 and NLRC4 inflammasomes contribute with ASC to acute brain injury independently of NLRP3

Abstract: Inflammation that contributes to acute cerebrovascular disease is driven by the proinflammatory cytokine interleukin-1 and is known to exacerbate resulting injury. The activity of interleukin-1 is regulated by multimolecular protein complexes called inflammasomes. There are multiple potential inflammasomes activated in diverse diseases, yet the nature of the inflammasomes involved in brain injury is currently unknown. Here, using a rodent model of stroke, we show that the NLRC4 (NLR family, CARD domain contain… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
3
2

Citation Types

16
242
2
1

Year Published

2015
2015
2024
2024

Publication Types

Select...
6
1

Relationship

0
7

Authors

Journals

citations
Cited by 234 publications
(261 citation statements)
references
References 55 publications
16
242
2
1
Order By: Relevance
“…During ischemic brain injury, a variety of processes such as ROS production, acidosis, K + efflux, etc., mediate the activation of the NLRP3 inflammasome and such altered physiological conditions also trigger the NLRP1 inflammasome (reviewed in [78]). NLRP3 was shown to mediate ischemic brain injury in a mouse model [79], which was later not confirmed [80]. Mice deficient in AIM2, NLRC4, or ASC had decreased infarct size and improved neurological scores and reduced activation of microglia and leukocyte recruitment, while the outcome of NLRP3 deficient mice was comparable to wild-type controls [80] in experimentally induced brain ischemia.…”
Section: Resultsmentioning
confidence: 97%
See 2 more Smart Citations
“…During ischemic brain injury, a variety of processes such as ROS production, acidosis, K + efflux, etc., mediate the activation of the NLRP3 inflammasome and such altered physiological conditions also trigger the NLRP1 inflammasome (reviewed in [78]). NLRP3 was shown to mediate ischemic brain injury in a mouse model [79], which was later not confirmed [80]. Mice deficient in AIM2, NLRC4, or ASC had decreased infarct size and improved neurological scores and reduced activation of microglia and leukocyte recruitment, while the outcome of NLRP3 deficient mice was comparable to wild-type controls [80] in experimentally induced brain ischemia.…”
Section: Resultsmentioning
confidence: 97%
“…NLRP3 was shown to mediate ischemic brain injury in a mouse model [79], which was later not confirmed [80]. Mice deficient in AIM2, NLRC4, or ASC had decreased infarct size and improved neurological scores and reduced activation of microglia and leukocyte recruitment, while the outcome of NLRP3 deficient mice was comparable to wild-type controls [80] in experimentally induced brain ischemia. These results are surprising when taking into account that NLRP3 is regarded as the main sensor of sterile injury, while NLRC4 activation is triggered by known PAMPs.…”
Section: Resultsmentioning
confidence: 97%
See 1 more Smart Citation
“…IL-18 also regulates IFN-γ signaling in T-cells and Natural Killer (NK) cells [60,76]. As previously mentioned, IL-18 can be activated through caspase-1 cleavage via inlammasome formation in addition to other proteases such as proteinase-3 [94].…”
Section: Inlammatory Cytokine-interleukin-18mentioning
confidence: 98%
“…While the reduction in caspase-1 and IL-1β activation via anti-NLRP1 in Abulaia's study evidences the role of NLRP1 in inlammasome formation post-stroke, it does not distinguish NLRP1's relative importance to other inlammasomes formed post-stroke. In a rodent model of stroke, the NLRC4 (NLR family, CARD domain containing 4) and AIM2 (absent in melanoma 2) inlammasomes were shown to contribute to brain injury without NLRP3 involvement (i.e., without this inlammasome commonly involved in brain injury) [58][59][60][61]. activation, decreased leukocyte recruitment and decreased infarct volume [59].…”
Section: The Inlammasome and Pro-inlammatory Cytokine Releasementioning
confidence: 99%