Cutting Edge: Reactive Oxygen Species Inhibitors Block Priming, but Not Activation, of the NLRP3 Inflammasome

By F. Bauernfeind, E. Bartok, Anna K Rieger, L. Franchi, G. Núñez, V. Hornung. Journal of Immunology, 2011

636 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/1e3081ee603abb5294ec6e72733ddb36929974cb

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology

1. T. Kanneganti
2. M. Lamkanfi
3. G. Núñez
4. V. Dixit
5. E. Latz
6. S. Man
7. Katherine A. Fitzgerald
8. Russell G. Jones

In Molecular Biology

1. T. Kanneganti
2. M. Lamkanfi
3. G. Núñez
4. S. Man
5. V. Dixit
6. Yuan He
7. E. Latz
8. H. Hara

Citations in the corpus

• CD36 coordinates NLRP3 inflammasome activation by facilitating the intracellular nucleation from soluble to particulate ligands in sterile inflammation (2013, background): “In the AD brain and diabetic pancreas, amyloid plaques arise from the aggregation of pre-fibrillar amyloidogenic peptides such as the Aβ(1-42) peptide17, 18, 19 or IAPP20, 21, 22, which oligomerize and give rise to higher order structures, including fibrils.”
• Mechanisms and functions of inflammasomes. (2014, background): “A single unifying event has not emerged because some of these events do not occur with all Nlrp3-activating agents, or they are associated with multiple inflammasomes, or their occurrence is contested (Bauernfeind et al., 2011; Muñoz-Planillo et al., 2013; Pétrilli et al., 2007).”
• The adapter MAVS promotes NLRP3 mitochondrial localization and inflammasome activation (2013, neutral): “…source of ROS and oxidized DNA required for NLRP3 activation (Nakahira et al., 2011; Shimada et al., 2012; Zhou et al., 2011); others indicate that ROS production is required for priming and transcriptional induction of NLRP3 expression, but not for NLRP3 activation (Bauernfeind et al., 2011).”
• Mechanism and regulation of NLRP3 inflammasome activation (2016, background): “At least one study showed that ROS inhibitors also affect the induction of NLRP3 at the priming stage when used at high concentrations [49].”
• The NLRP3 Inflammasome: An Overview of Mechanisms of Activation and Regulation (2019, background): “At least one study reported that ROS inhibitors also block the priming signal for NLRP3 inflammasome activation [100].”
• Itaconate Links Inhibition of Succinate Dehydrogenase with Macrophage Metabolic Remodeling and Regulation of Inflammation (2016, background): “As interfering with mROS can affect inflammasome priming (Bauernfeind et al., 2011), the blunted mROS response mechanistically links Sdh inhibition and the anti-inflammatory effects of itaconate on IL-1b and IL-18 production (Figure 1G).”
• The Reactive Oxygen Species in Macrophage Polarization: Reflecting Its Dual Role in Progression and Treatment of Human Diseases (2016, background): “in inflammasome activation is far more complicated as postulated and studies reported on caspase-8-dependent inflammasome activation and ROS-induced NLRP3 inflammasome priming have been further proposed recently [118, 119].”
• Inflammasomes and their roles in health and disease. (2012, background): “Inflammasome components such as NLRP3, caspase-11, and proIL-1β are expressed at relatively low levels, and priming with NFκB-activating inflammatory cytokines, TLR ligands, and other PAMPs is required for their mRNAs to be induced (Bauernfeind et al. 2011, Bulua et al. 2011, Kayagaki et al. 2011).”
• Regulation of inflammasome activation (2015, background): “A number of studies argued that mitochondrial perturbation, ROS, formation of large membrane pores and cell volume fluctuation are not required for the activation of the canonical NLRP3 inflammasome (53, 61, 62).”