The DOI matches its Crossref record; 26 of the 27 references it cites were found in a registry or an index; none of the 35 sources its claims cite is checked for support yet.
Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica
Open accessAbstract
The inhalation of airborne pollutants, such as asbestos or silica, is linked to inflammation of the lung, fibrosis, and lung cancer. How the presence of pathogenic dust is recognized and how chronic inflammatory diseases are triggered are poorly understood. Here, we show that asbestos and silica are sensed by the Nalp3 inflammasome, whose subsequent activation leads to interleukin-1β secretion. Inflammasome activation is triggered by reactive oxygen species, which are generated by a NADPH oxidase upon particle phagocytosis. (NADPH is the reduced form of nicotinamide adenine dinucleotide phosphate.) In a model of asbestos inhalation, Nalp3 –/– mice showed diminished recruitment of inflammatory cells to the lungs, paralleled by lower cytokine production. Our findings implicate the Nalp3 inflammasome in particulate matter–related pulmonary diseases and support its role as a major proinflammatory “danger” receptor.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
0 of 35 cited sources checked · 0 supported · 0 flagged
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“We inhibited K + efflux by adding high concentrations (130 mM) of KCl to the culture media of THP1 cells and found that asbestos-induced IL-1β production was blocked (Fig. 3A).”
§ Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Rests on an assumption: The inhibitors used (cytochalasin D, latrunculin A, KCl, NAC, APDC, DPI, apocynin, deferoxamine, uricase) act specifically on their intended targets without off-target effects that explain the results.
None of the sources cited for this claim have been checked yet.
In the paper
“By contrast, IL-1β production was independent of the Ipaf inflammasome, which has been shown to activate caspase-1 and produce IL-1β in response to flagellin from Salmonella typhimurium and Legionella pneumophila (fig.S4) (11,12).”
§ Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica > Abstract
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Primary human monocyte-derived macrophages also produced mature IL-1β after stimulation with asbestos or silica (Fig. 1C), while DEP exposure again did not result in IL-1β secretion.”
§ Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica > Abstract
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Rests on an assumption: THP1 cells and primary human monocyte-derived macrophages respond to particulate stimulation in a way that represents human alveolar macrophages in vivo.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“IL-1β production was indeed impaired in response to asbestos, MSU and ATP when using these inhibitors (Fig. 3D), suggesting that ROS production was a necessary step in inflammasome activation.”
§ Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Rests on an assumption: The inhibitors used (cytochalasin D, latrunculin A, KCl, NAC, APDC, DPI, apocynin, deferoxamine, uricase) act specifically on their intended targets without off-target effects that explain the results.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“However, significantly fewer cells were recruited to the lungs of Nalp3 -/- mice after exposure to asbestos (Fig. 4A).”
§ Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Rests on an assumption: The mouse model of asbestos inhalation reflects the human pulmonary inflammatory response sufficiently to infer human disease mechanisms.
- Rests on an assumption: Nalp3-deficient mice lack Nalp3 inflammasome function without compensatory developmental or immunological alterations that affect the measured outcomes.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“KC, a potent neutrophil chemoattractant, and IL-1β were decreased in Nalp3 -/-mice, whereas IL-12(p40) production was independent of Nalp3.”
§ Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Rests on an assumption: The mouse model of asbestos inhalation reflects the human pulmonary inflammatory response sufficiently to infer human disease mechanisms.
- Rests on an assumption: Nalp3-deficient mice lack Nalp3 inflammasome function without compensatory developmental or immunological alterations that affect the measured outcomes.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“To clarify this, we determined whether the particulates activate caspase-1 in THP1 cells and indeed found processing of caspase-1 into the p10 fragment (fig.S1).”
§ Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Rests on an assumption: THP1 cells and primary human monocyte-derived macrophages respond to particulate stimulation in a way that represents human alveolar macrophages in vivo.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“We indeed observed that the macrophage-like cell line THP1 secreted mature IL-1β upon stimulation with asbestos or silica (Fig. 1A).”
§ Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Rests on an assumption: THP1 cells and primary human monocyte-derived macrophages respond to particulate stimulation in a way that represents human alveolar macrophages in vivo.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“To further corroborate NADPH oxidase as a source of ROS production, we knocked down the common NADPH oxidase subunit p22phox and found highly diminished IL-1β secretion (Fig. 3F).”
§ Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Rests on an assumption: THP1 cells and primary human monocyte-derived macrophages respond to particulate stimulation in a way that represents human alveolar macrophages in vivo.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The same effect was achieved by treating the cells with the inhibitor of actin polymerisation, latrunculin A (fig.S5).”
§ Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica > Abstract
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Rests on an assumption: The inhibitors used (cytochalasin D, latrunculin A, KCl, NAC, APDC, DPI, apocynin, deferoxamine, uricase) act specifically on their intended targets without off-target effects that explain the results.
- It may state two separate claims as one. 17
- Probably not a substantial claim. 10
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Here, we show that asbestos and silica are sensed by the Nalp3 inflammasome, whose subsequent activation leads to interleukin 1β secretion.”
§ Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: THP1 cells and primary human monocyte-derived macrophages respond to particulate stimulation in a way that represents human alveolar macrophages in vivo.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In support of this, ROS production was inhibited by the NADPH oxidase inhibitors diphenylene iodonium (DPI) and apocynin, but not with rotenone (an inhibitor of mitochondrial complex I) or TTFA (an inhibitor of mitochondrial complex II) (fig.S7).”
§ Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: The inhibitors used (cytochalasin D, latrunculin A, KCl, NAC, APDC, DPI, apocynin, deferoxamine, uricase) act specifically on their intended targets without off-target effects that explain the results.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Caspase-1 was no longer cleaved and secreted in the presence of the pan-caspase inhibitor zVAD or in macrophages from Nalp3 and ASC deficient mice and as a consequence, mature IL-1β processing and secretion was abolished (Fig. 2B).”
§ Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: Nalp3-deficient mice lack Nalp3 inflammasome function without compensatory developmental or immunological alterations that affect the measured outcomes.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“We observed that iron chelation of asbestos fibres by deferoxamine strongly reduced IL-1β maturation, whereas it had no effect in response to MSU crystals (Fig. 3E).”
§ Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: The inhibitors used (cytochalasin D, latrunculin A, KCl, NAC, APDC, DPI, apocynin, deferoxamine, uricase) act specifically on their intended targets without off-target effects that explain the results.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In a model of asbestos inhalation, Nalp3 -/-mice showed diminished recruitment of inflammatory cells to the lungs, paralleled by lower cytokine production.”
§ Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: The mouse model of asbestos inhalation reflects the human pulmonary inflammatory response sufficiently to infer human disease mechanisms.
- Rests on an assumption: Nalp3-deficient mice lack Nalp3 inflammasome function without compensatory developmental or immunological alterations that affect the measured outcomes.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“On the other hand, uricase treatment blocked the activity of MSU but not of asbestos.”
§ Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: The inhibitors used (cytochalasin D, latrunculin A, KCl, NAC, APDC, DPI, apocynin, deferoxamine, uricase) act specifically on their intended targets without off-target effects that explain the results.
None of the sources cited for this claim have been checked yet.
In the paper
“The Nalp3 inflammasome is implicated in the pathological increase of IL-1β production in autoinflammatory syndromes, such as Muckle-Wells syndrome (22), as well as inflammatory processes, such as gout and pseudogout (7).”
§ Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica > Abstract
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Likewise inflammatory responses are observed after exposure to other particulates such as found in diesel exhaust (5).”
§ Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica > Abstract
What the sources say
- Not checked yetcites [5] source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Our findings implicate the Nalp3 inflammasome in particulate matter-related pulmonary diseases and support its role as a major proinflammatory”
§ Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: The mouse model of asbestos inhalation reflects the human pulmonary inflammatory response sufficiently to infer human disease mechanisms.
- Rests on an assumption: THP1 cells and primary human monocyte-derived macrophages respond to particulate stimulation in a way that represents human alveolar macrophages in vivo.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Our findings support the implication of the Nalp3 inflammasome in pulmonary inflammatory diseases that are linked to pathogenic air pollutants and can ultimately lead to lung cancer and fibrosis.”
§ Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: The mouse model of asbestos inhalation reflects the human pulmonary inflammatory response sufficiently to infer human disease mechanisms.
- Rests on an assumption: THP1 cells and primary human monocyte-derived macrophages respond to particulate stimulation in a way that represents human alveolar macrophages in vivo.
None of the sources cited for this claim have been checked yet.
In the paper
“In addition to PAMPs, Nalp3 has the extraordinary capacity of sensing endogenous stress-associated danger signals (DAMPs) such as ATP (9) or MSU (7).”
§ Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica > Abstract
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Models of asbestos inhalation have revealed that the airway epithelium and alveolar macrophages play important roles in cell proliferation, inflammation and fibrogenesis triggered by the asbestos fibres (reviewed in (1)).”
§ Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica > Abstract
What the sources say
- Not checked yetcites [1] source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Crocidolite asbestos fibres appear to be particularly potent ROS producers due to the presence of iron on the fibre surface.The iron is thought to play an important role in the generation of free radicals (3).”
§ Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica > Abstract
What the sources say
- Not checked yetcites [3] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Asbestos fibres have been associated with development of malignant mesotheliomas after environmental exposures (2).”
§ Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica > Abstract
What the sources say
- Not checked yetcites [2] source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Since the mature form of IL-1β did not accumulate inside the cell (Fig. 3C), we conclude that the actin cytoskeleton is necessary for the attempt to phagocytose, and not to drive mature IL-1β secretion.”
§ Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: The inhibitors used (cytochalasin D, latrunculin A, KCl, NAC, APDC, DPI, apocynin, deferoxamine, uricase) act specifically on their intended targets without off-target effects that explain the results.
None of the sources cited for this claim have been checked yet.
In the paper
“Recent data also suggest a role for ROS in activating caspase-1 upon ATP treatment (18) and in Nalp3 inflammasome activation by MSU and R837 (13).”
§ Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. It may state two separate claims as one.
In the paper
“Phagocytic cells can endocytose small particles, whereas bigger crystals or fibres are subject to so-called”
§ Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica > Abstract
What the sources say
- Not checked yetcites [16]
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Inhalation of asbestos or silica in occupational exposures can result in pulmonary fibrosis (asbestosis, silicosis), and lung cancer, especially in smokers (1).”
§ Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica > Abstract
What the sources say
- Not checked yetcites [1] source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“An important role for IL-1β has been proposed in the pathogenesis of asbestos-induced mesothelioma by regulating human mesothelial cell proliferation (23) and IL-1β-driven inflammation is well known to promote the development and invasiveness of several tumour types in vivo (24).”
§ Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica > Abstract
What the sources say
- Not checked yetcites [23]
- Not checked yetcites [24] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. It may state two separate claims as one.
In the paper
“The Nalp3 inflammasome, composed of the Nod-like receptor (NLR) protein Nalp3 (Cryopyrin/NLRP3), Cardinal, the adaptor ASC and caspase-1, is implicated in the production of mature IL-1β in response to a variety of signals.”
§ Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica > Abstract
What the sources say
- Not checked yetcites [8] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Asbestos, MSU and probably other particles activate the NALP3 inflammasome in a similar way, requiring actin-mediated cellular uptake in contrast to small, non-particulate molecules such as R837, ATP or nigericin.”
§ Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: THP1 cells and primary human monocyte-derived macrophages respond to particulate stimulation in a way that represents human alveolar macrophages in vivo.
None of the sources cited for this claim have been checked yet.
In the paper
“For example, the presence of bacteria is recognized through binding of the pathogen-associated molecular pattern (PAMP) muramyldipeptide (MDP) or via the action of bacterial toxins (9,10).”
§ Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica > Abstract
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“Asbestos fibres have been shown to participate in redox reactions to generate reactive oxygen species (ROS) that are widely linked to signalling pathways causing inflammation and carcinogenesis [reviewed in (17)].”
§ Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica > Abstract
What the sources say
- Not checked yetcites [17] source
Strength:boosted· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
The paper relies on this without support.
The mouse model of asbestos inhalation reflects the human pulmonary inflammatory response sufficiently to infer human disease mechanisms.
“To investigate the in vivo significance of the Nalp3 inflammasome in asbestos-induced inflammation, Nalp3 -/-and Nalp3 +/+ littermate mice were exposed for 9 days to chrysotile asbestos and markers of injury, inflammation and cytokine production were analysed on day 10.”
“Our findings support the implication of the Nalp3 inflammasome in pulmonary inflammatory diseases that are linked to pathogenic air pollutants and can ultimately lead to lung cancer and fibrosis.”
The paper relies on this without support.
The in vitro concentrations and exposure durations of asbestos and silica used in cell culture are relevant to human exposures.
“THP1 cells were stimulated for 6 h with the indicated amounts (mg/ml media) of asbestos, silica, diesel exhaust particles (DEP), cigarette smoke extract (CSE, in % solution) and MSU.”
“Primary human monocyte-derived macrophages also produced mature IL-1β after stimulation with asbestos or silica (Fig. 1C)”
The paper relies on this without support.
Nalp3-deficient mice lack Nalp3 inflammasome function without compensatory developmental or immunological alterations that affect the measured outcomes.
“Nalp3 -/-and Nalp3 +/+ littermate mice were exposed for 9 days to chrysotile asbestos and markers of injury, inflammation and cytokine production were analysed on day 10.”
“However, significantly fewer cells were recruited to the lungs of Nalp3 -/- mice after exposure to asbestos (Fig. 4A).”
The paper relies on this without support.
The inhibitors used (cytochalasin D, latrunculin A, KCl, NAC, APDC, DPI, apocynin, deferoxamine, uricase) act specifically on their intended targets without off-target effects that explain the results.
“Cytochalasin D inhibited not only secretion of mature IL-1β by asbestos (Fig. 3C), but also by the particulate MSU, while for non-crystalline Nalp3 activators such as R837 and nigericin, IL-1β secretion was not affected (Fig. 3C).”
“IL-1β production was indeed impaired in response to asbestos, MSU and ATP when using these inhibitors (Fig. 3D), suggesting that ROS production was a necessary step in inflammasome activation.”
The paper relies on this without support.
THP1 cells and primary human monocyte-derived macrophages respond to particulate stimulation in a way that represents human alveolar macrophages in vivo.
“We indeed observed that the macrophage-like cell line THP1 secreted mature IL-1β upon stimulation with asbestos or silica (Fig. 1A).”
“Primary human monocyte-derived macrophages also produced mature IL-1β after stimulation with asbestos or silica (Fig. 1C)”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“In the second, activation step, the now primed NLRP3 inflammasome can be directly activated by any of the various signals including ATP, reactive oxygen species (ROS) and DNA released from damaged mitochondria, protein aggregates, uric acid crystals and ceramide, bacterial or viral RNA, airborne pollutants such as asbestos and silica, decreased intracellular concentrations of K+ and Cl− as well as”
From Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease (2023) · cites this paper as [60]
Experimental — accuracy not yet measuredIn the citing paper
“These results suggest that mtROS serve as direct activators of the NLRP3 inflammasome.”
From Trimethylamine‐N‐Oxide Induces Vascular Inflammation by Activating the NLRP3 Inflammasome Through the SIRT3‐SOD2‐mtROS Signaling Pathway (2017) · cites this paper as [37]
In the citing paper
“Conversely, treatment with ROS inhibitors has been shown to suppress cadmium‐, silica‐, and asbestos‐induced NLRP3 inflammasome activation.37, 38”
From Trimethylamine‐N‐Oxide Induces Vascular Inflammation by Activating the NLRP3 Inflammasome Through the SIRT3‐SOD2‐mtROS Signaling Pathway (2017) · cites this paper as [37]
In the citing paper
“Inhalation of crystalline silica can induce inflammation by stimulating the NLRP3 inflammasome, a cytosolic receptor complex that plays a critical role in driving inflammatory immune responses.”
From Volcanic Ash Activates the NLRP3 Inflammasome in Murine and Human Macrophages (2018) · cites this paper as [19]
In the citing paper
“Particulate substances or fibers are likely candidates for the initiation of ROS (19).”
From Volcanic Ash Activates the NLRP3 Inflammasome in Murine and Human Macrophages (2018) · cites this paper as [19]
In the citing paper
“Consistently, in mouse models of sterile injury, such as gout, asbestosis and silicosis, NLRP3-deficient mice exhibited decreased inflammation with reduced levels of tissue infiltration by neutrophils or macrophages55,57,58.”
From Sterile inflammation: sensing and reacting to damage (2010) · cites this paper as [57]
In the citing paper
“Silica58,68, asbestos57 and ATP69 have all been associated with ROS production, and ROS inhibition in vitro resulted in impairment of caspase 1 activation and IL-1β production by these stimuli57,58,69.”
From Sterile inflammation: sensing and reacting to damage (2010) · cites this paper as [57]
Citations
Cites
Martinon, F., Burns, K., & Tschopp, J. (2002) · Molecular Cell · doi:10.1016/s1097-2765(02)00599-3 · Cited by 6,066
Self-citationGout-associated uric acid crystals activate the NALP3 inflammasome
Martinon, F., Pétrilli, V., Mayor, A., Tardivel, A., & Tschopp, J. (2006) · Nature · doi:10.1038/nature04516 · Cited by 5,326
Self-citationCryopyrin activates the inflammasome in response to toxins and ATP
Mariathasan, S., Weiss, D. S., Newton, K., McBride, J., O'Rourke, K., Roose-Girma, M., Lee, W. P., Weinrauch, Y., Monack, D. M., & Dixit, V. M. (2006) · Nature · doi:10.1038/nature04515 · Cited by 3,080
Agostini, L., Martinon, F., Burns, K., McDermott, M. F., Hawkins, P. N., & Tschopp, J. (2004) · Immunity · doi:10.1016/s1074-7613(04)00046-9 · Cited by 1,768
Self-citationActivation of the NALP3 inflammasome is triggered by low intracellular potassium concentration
Pétrilli, V, Papin, S., Dostert, C., Mayor, A., Martinon, F., & Tschopp, J. (2007) · Cell Death & Differentiation · doi:10.1038/sj.cdd.4402195 · Cited by 1,445
Self-citationCytoplasmic flagellin activates caspase-1 and secretion of interleukin 1β via Ipaf
Miao, E. A., Alpuche-Aranda, C. M., Dors, M., Clark, A. E., Bader, M. W., Miller, S. I., & Aderem, A. (2006) · Nature Immunology · doi:10.1038/ni1344 · Cited by 1,127
Fernandes-Alnemri, T., Wu, J., Yu, J.-W., Datta, P., Miller, B., Jankowski, W., Rosenberg, S., Zhang, J., & Alnemri, E. S. (2007) · Cell Death & Differentiation · doi:10.1038/sj.cdd.4402194 · Cited by 1,026
Mechanisms in the Pathogenesis of Asbestosis and Silicosis
MOSSMAN, B. T., & CHURG, A. (1998) · American Journal of Respiratory and Critical Care Medicine · doi:10.1164/ajrccm.157.5.9707141 · Cited by 971
Self-citationCruz, C. M., Rinna, A., Forman, H. J., Ventura, A. L. M., Persechini, P. M., & Ojcius, D. M. (2007) · Journal of Biological Chemistry · doi:10.1074/jbc.m608083200 · Cited by 786
Asbestos: Scientific Developments and Implications for Public Policy
Mossman, B. T., Bignon, J., Corn, M., Seaton, A., & Gee, J. B. L. (1990) · Science · doi:10.1126/science.2153315 · Cited by 742
Self-citation
Flagged first, then by citations
1 of the 27 references couldn’t be matched to a known paper.
Research works printed but not linked: 2
- K. Hansen, B. T. Mossman, Cancer Res.47, 1681 (1987).
- Y. Wanget al., Int. J. Oncol.25, 173 (2004).
Cited by
Sorted by citations
Immunity, Inflammation, and Cancer
Grivennikov, S. I., Greten, F. R., & Karin, M. (2010) · Cell · doi:10.1016/j.cell.2010.01.025 · Cited by 10,755
“Such particles, however, can trigger inflammation through effects on prointerluekin-1β (IL-1β) processing by the inflammasome (Dostert et al., 2008) and this may mediate their tumorigenic activity.”
ROS function in redox signaling and oxidative stress
Schieber, M., & Chandel, N. S. (2014) · Current Biology · doi:10.1016/j.cub.2014.03.034 · Cited by 6,931
Brook, R. D., Rajagopalan, S., Pope, C. A., Brook, J. R., Bhatnagar, A., Diez-Roux, A. V., Holguin, F., Hong, Y., Luepker, R. V., Mittleman, M. A., et al. (2010) · Circulation · doi:10.1161/cir.0b013e3181dbece1 · Cited by 6,548
Origin and physiological roles of inflammation
Medzhitov, R. (2008) · Nature · doi:10.1038/nature07201 · Cited by 6,618
A role for mitochondria in nlrp3 inflammasome activation
Zhou, R., Yazdi, A. S., Menu, P., & Tschopp, J. (2011) · Nature · doi:10.1038/nature09663 · Cited by 5,602
Self-citationSchroder, K., & Tschopp, J. (2010) · Cell · doi:10.1016/j.cell.2010.01.040 · Cited by 5,475
“This Review focuses on those PRRs that assemble into high-molecular weight, caspase-1-activating platforms called ‘‘inflamma-somes’’ that control maturation and secretion of interleukins such asIL-1 b and IL-18, whose potent proinflammatory activities direct host responses to infection and injury.”
InfluentialSelf-citationRole of nrf2 in oxidative stress and toxicity
Ma, Q. (2013) · Annual Review of Pharmacology and Toxicology · doi:10.1146/annurev-pharmtox-011112-140320 · Cited by 4,903
Reactive Oxygen Species in Inflammation and Tissue Injury
Mittal, M., Siddiqui, M. R., Tran, K., Reddy, S. P., & Malik, A. B. (2014) · Antioxidants & Redox Signaling · doi:10.1089/ars.2012.5149 · Cited by 4,897
“NLRP3 inflammasome, the most well-characterized form, is redox sensitive (99, 379).”
The NLRP3 inflammasome: molecular activation and regulation to therapeutics
Swanson, K. V., Deng, M., & Ting, J. P.-Y. (2019) · Nature Reviews Immunology · doi:10.1038/s41577-019-0165-0 · Cited by 4,884
NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals
Duewell, P., Kono, H., Rayner, K. J., Sirois, C. M., Vladimer, G., Bauernfeind, F. G., Abela, G. S., Franchi, L., Nuñez, G., Schnurr, M., et al. (2010) · Nature · doi:10.1038/nature08938 · Cited by 4,026
The NLRP3 Inflammasome: an overview of mechanisms of activation and regulation
Kelley, N., Jeltema, D., Duan, Y., & He, Y. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20133328 · Cited by 3,539
Pyroptosis: host cell death and inflammation
Bergsbaken, T., Fink, S. L., & Cookson, B. T. (2009) · Nature Reviews Microbiology · doi:10.1038/nrmicro2070 · Cited by 3,288
Nakahira, K., Haspel, J. A., Rathinam, V. A. K., Lee, S.-J., Dolinay, T., Lam, H. C., Englert, J. A., Rabinovitch, M., Cernadas, M., Kim, H. P., et al. (2011) · Nature Immunology · doi:10.1038/ni.1980 · Cited by 3,049
“Crystalline particles such as asbestos, silica and monosodium urate have been shown to activate the NALP3 inflammasome through ROS generation induced by phagocytic NADPH oxidas”
Hornung, V., Bauernfeind, F., Halle, A., Samstad, E. O., Kono, H., Rock, K. L., Fitzgerald, K. A., & Latz, E. (2008) · Nature Immunology · doi:10.1038/ni.1631 · Cited by 3,065
Sterile inflammation: sensing and reacting to damage
Chen, G. Y., & Nuñez, G. (2010) · Nature Reviews Immunology · doi:10.1038/nri2873 · Cited by 3,051
Activation and regulation of the inflammasomes
Latz, E., Xiao, T. S., & Stutz, A. (2013) · Nature Reviews Immunology · doi:10.1038/nri3452 · Cited by 2,884
Mechanism and Regulation of NLRP3 Inflammasome Activation
He, Y., Hara, H., & Núñez, G. (2016) · Trends in Biochemical Sciences · doi:10.1016/j.tibs.2016.09.002 · Cited by 2,759
Thioredoxin-interacting protein links oxidative stress to inflammasome activation
Zhou, R., Tardivel, A., Thorens, B., Choi, I., & Tschopp, J. (2010) · Nature Immunology · doi:10.1038/ni.1831 · Cited by 2,708
Self-citationThe NLRP3 inflammasome instigates obesity-induced inflammation and insulin resistance
Vandanmagsar, B., Youm, Y.-H., Ravussin, A., Galgani, J. E., Stadler, K., Mynatt, R. L., Ravussin, E., Stephens, J. M., & Dixit, V. D. (2011) · Nature Medicine · doi:10.1038/nm.2279 · Cited by 2,655
Physiological Roles of Mitochondrial Reactive Oxygen Species
Sena, L. A., & Chandel, N. S. (2012) · Molecular Cell · doi:10.1016/j.molcel.2012.09.025 · Cited by 2,632
Caspase Functions in Cell Death and DiseasePreprint
McIlwain, D. R., Berger, T., & Mak, T. W. (2013) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a008656 · Cited by 2,702
Yunna, C., Mengru, H., Lei, W., & Weidong, C. (2020) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2020.173090 · Cited by 2,454
The NALP3 inflammasome is involved in the innate immune response to amyloid-β
Halle, A., Hornung, V., Petzold, G. C., Stewart, C. R., Monks, B. G., Reinheckel, T., Fitzgerald, K. A., Latz, E., Moore, K. J., & Golenbock, D. T. (2008) · Nature Immunology · doi:10.1038/ni.1636 · Cited by 2,441
The Inflammasomes: Guardians of the Body
Martinon, F., Mayor, A., & Tschopp, J. (2009) · Annual Review of Immunology · doi:10.1146/annurev.immunol.021908.132715 · Cited by 2,436
Self-citationInflammasomes in health and disease
Strowig, T., Henao-Mejia, J., Elinav, E., & Flavell, R. (2012) · Nature · doi:10.1038/nature10759 · Cited by 2,230
Nathan, C., & Ding, A. (2010) · Cell · doi:10.1016/j.cell.2010.02.029 · Cited by 2,183
Loss of the autophagy protein Atg16L1 enhances endotoxin-induced IL-1β production
Saitoh, T., Fujita, N., Jang, M. H., Uematsu, S., Yang, B., Satoh, T., Omori, H., Noda, T., Yamamoto, N., Komatsu, M., et al. (2008) · Nature · doi:10.1038/nature07383 · Cited by 2,064
Targeting the NLRP3 inflammasome in inflammatory diseases
Mangan, M. S. J., Olhava, E. J., Roush, W. R., Seidel, H. M., Glick, G. D., & Latz, E. (2018) · Nature Reviews Drug Discovery · doi:10.1038/nrd.2018.97 · Cited by 1,885
Franchi, L., Eigenbrod, T., Muñoz-Planillo, R., & Nuñez, G. (2009) · Nature Immunology · doi:10.1038/ni.1703 · Cited by 1,834
NLRP3 inflammasome activation: the convergence of multiple signalling pathways on ROS production?
Tschopp, J., & Schroder, K. (2010) · Nature reviews. Immunology · doi:10.1038/nri2725 · Cited by 1,859
Self-citationAIM2 activates the inflammasome and cell death in response to cytoplasmic DNA
Fernandes-Alnemri, T., Yu, J.-W., Datta, P., Wu, J., & Alnemri, E. S. (2009) · Nature · doi:10.1038/nature07710 · Cited by 1,831
The roles of TLRs, RLRs and NLRs in pathogen recognition
Kawai, T., & Akira, S. (2009) · International Immunology · doi:10.1093/intimm/dxp017 · Cited by 1,725
Beyond oxidative stress: an immunologist's guide to reactive oxygen species
Nathan, C., & Cunningham-Bussel, A. (2013) · Nature Reviews Immunology · doi:10.1038/nri3423 · Cited by 1,619
The Inflammasome NLRs in Immunity, Inflammation, and Associated Diseases
Davis, B. K., Wen, H., & Ting, J. P.-Y. (2011) · Annual Review of Immunology · doi:10.1146/annurev-immunol-031210-101405 · Cited by 1,618
Molecular mechanisms regulating NLRP3 inflammasome activation
Jo, E.-K., Kim, J. K., Shin, D.-M., & Sasakawa, C. (2016) · Cellular & Molecular Immunology · doi:10.1038/cmi.2015.95 · Cited by 1,378
Ridker, P. M., MacFadyen, J. G., Thuren, T., Everett, B. M., Libby, P., Glynn, R. J., Ridker, P., Lorenzatti, A., Krum, H., Varigos, J., et al. (2017) · The Lancet · doi:10.1016/s0140-6736(17)32247-x · Cited by 1,344
Masters, S. L., Dunne, A., Subramanian, S. L., Hull, R. L., Tannahill, G. M., Sharp, F. A., Becker, C., Franchi, L., Yoshihara, E., Chen, Z., et al. (2010) · Nature Immunology · doi:10.1038/ni.1935 · Cited by 1,330
Integrating mechanisms of pulmonary fibrosis
Wynn, T. A. (2011) · The Journal of Experimental Medicine · doi:10.1084/jem.20110551 · Cited by 1,326
Innate immunity to virus infection
Takeuchi, O., & Akira, S. (2008) · Immunological Reviews · doi:10.1111/j.1600-065x.2008.00737.x · Cited by 1,269
Reactive oxygen species and mitochondria: A nexus of cellular homeostasis
Dunn, J. D., Álvarez, L., Zhang, X., & Soldati, T. (2015) · Redox Biology · doi:10.1016/j.redox.2015.09.005 · Cited by 1,233
“Initial studies focused on NOX2 as the relevant ROS source: inhibition or knockdown of NOX2 were found to block IL-1β secretion in response to NLRP3 stimuli [105,109,131].”
BackgroundLeung, C. C., Yu, I. T. S., & Chen, W. (2012) · The Lancet · doi:10.1016/s0140-6736(12)60235-9 · Cited by 1,193
The NLRP3 Inflammasome: A Sensor for Metabolic Danger?
Schroder, K., Zhou, R., & Tschopp, J. (2010) · Science · doi:10.1126/science.1184003 · Cited by 1,153
Self-citationAllen, I. C., Scull, M. A., Moore, C. B., Holl, E. K., McElvania-TeKippe, E., Taxman, D. J., Guthrie, E. H., Pickles, R. J., & Ting, J. P.-Y. (2009) · Immunity · doi:10.1016/j.immuni.2009.02.005 · Cited by 1,113
Regulation of inflammasome activation
Man, S. M., & Kanneganti, T. (2015) · Immunological Reviews · doi:10.1111/imr.12296 · Cited by 1,088
Horror Autoinflammaticus: The Molecular Pathophysiology of Autoinflammatory Disease
Masters, S. L., Simon, A., Aksentijevich, I. A., & Kastner, D. L. (2009) · Annual Review of Immunology · doi:10.1146/annurev.immunol.25.022106.141627 · Cited by 1,083
Inflammasome activation and regulation: toward a better understanding of complex mechanisms
Zheng, D., Liwinski, T., & Elinav, E. (2020) · Cell Discovery · doi:10.1038/s41421-020-0167-x · Cited by 1,078
Rajamäki, K., Lappalainen, J., Öörni, K., Välimäki, E., Matikainen, S., Kovanen, P. T., & Eklund, K. K. (2010) · PLoS ONE · doi:10.1371/journal.pone.0011765 · Cited by 1,039
Sensing and reacting to microbes through the inflammasomes
Franchi, L., Muñoz-Planillo, R., & Núñez, G. (2012) · Nature Immunology · doi:10.1038/ni.2231 · Cited by 1,046
Mitochondria in the Regulation of Innate and Adaptive Immunity
Weinberg, S. E., Sena, L. A., & Chandel, N. S. (2015) · Immunity · doi:10.1016/j.immuni.2015.02.002 · Cited by 960
“Diverse PAMPs and DAMPs such as lipopolysaccharide (LPS), asbestos, ATP, and uric acid lead to NLRP3 activation through increase in ROS (Cruz et al., 2007; Dostert et al., 2008).”
NLRP3 Inflammasome and the IL-1 Pathway in Atherosclerosis
Grebe, A., Hoss, F., & Latz, E. (2018) · Circulation Research · doi:10.1161/circresaha.118.311362 · Cited by 926
Redox Regulation of NLRP3 Inflammasomes: ROS as Trigger or Effector?
Abais, J. M., Xia, M., Zhang, Y., Boini, K. M., & Li, P. (2014) · Antioxidants and Redox Signaling · doi:10.1089/ars.2014.5994 · Cited by 936
“The first study of this kind demonstrated inhibited caspase-1 activation and IL-1b release in monocyte THP-1 cells in response to asbestos, MSU, and silica on specific knockdown of NADPH oxidase subunit p22 or use of general ROS scavengers such as N-acetylcysteine and antioxidant ammonium pyrrolidine dithiocarbamate (…”
InfluentialMitochondrial dysfunction in pathophysiology of heart failure
Zhou, B., & Tian, R. (2018) · Journal of Clinical Investigation · doi:10.1172/jci120849 · Cited by 973
Syk kinase signalling couples to the Nlrp3 inflammasome for anti-fungal host defence
Groß, O., Poeck, H., Bscheider, M., Dostert, C., Hannesschläger, N., Endres, S., Hartmann, G., Tardivel, A., Schweighoffer, E., Tybulewicz, V. L. J., et al. (2009) · Nature · doi:10.1038/nature07965 · Cited by 947
Self-citationMitochondrial Cardiolipin Is Required for Nlrp3 Inflammasome Activation
Iyer, S. S., He, Q., Janczy, J. R., Elliott, E. I., Zhong, Z., Olivier, A. K., Sadler, J. J., Knepper-Adrian, V., Han, R., Qiao, L., et al. (2013) · Immunity · doi:10.1016/j.immuni.2013.08.001 · Cited by 968
Colitis induced in mice with dextran sulfate sodium (DSS) is mediated by the NLRP3 inflammasome
Bauer, C. A., Duewell, P., Mayer, C., Lehr, H. A., Fitzgerald, K. A., Dauer, M., Tschopp, J., Endres, S., Latz, E., & Schnurr, M. M. (2010) · Gut · doi:10.1136/gut.2009.197822 · Cited by 928
Self-citationFunction of Nod‐like receptors in microbial recognition and host defense
Franchi, L., Warner, N. E., Viani, K. L., & Núñez, G. (2008) · Immunological Reviews · doi:10.1111/j.1600-065x.2008.00734.x · Cited by 938
The Sterile Inflammatory Response
Rock, K. L., Latz, E., Ontiveros, F., & Kono, H. (2010) · Annual Review of Immunology · doi:10.1146/annurev-immunol-030409-101311 · Cited by 865
Towards an understanding of the adjuvant action of aluminium
Marrack, P., McKee, A. S., & Munks, M. W. (2009) · Nature Reviews Immunology · doi:10.1038/nri2510 · Cited by 887
“Related reports have shown that other particulate materials, such as silica, asbestos and MSU crystals, also act through the NLRP3 inflammasome to produce IL-1&beta”
Kawaguchi, M., Takahashi, M., Hata, T., Kashima, Y., Usui, F., Morimoto, H., Izawa, A., Takahashi, Y., Masumoto, J., Koyama, J., et al. (2011) · Circulation · doi:10.1161/circulationaha.110.982777 · Cited by 884
DAMPs, PAMPs, and LAMPs in Immunity and Sterile Inflammation
Zindel, J., & Kubes, P. (2019) · Annual Review of Pathology Mechanisms of Disease · doi:10.1146/annurev-pathmechdis-012419-032847 · Cited by 915
Microtubule-driven spatial arrangement of mitochondria promotes activation of the NLRP3 inflammasome
Misawa, T., Takahama, M., Kozaki, T., Lee, H., Zou, J., Saitoh, T., & Akira, S. (2013) · Nature Immunology · doi:10.1038/ni.2550 · Cited by 894
Bulua, A. C., Simon, A., Maddipati, R., Pelletier, M., Park, H., Kim, K.-Y., Sack, M. N., Kastner, D. L., & Siegel, R. M. (2011) · Journal of Experimental Medicine · doi:10.1084/jem.20102049 · Cited by 860
Pathogenic Mechanisms Underlying Idiopathic Pulmonary Fibrosis
Moss, B. J., Ryter, S. W., & Rosas, I. O. (2021) · Annual Review of Pathology Mechanisms of Disease · doi:10.1146/annurev-pathol-042320-030240 · Cited by 852
Beutler, B. A. (2009) · Blood · doi:10.1182/blood-2008-07-019307 · Cited by 840
Reactive oxygen species in health and disease
Alfadda, A. A., & Sallam, R. M. (2012) · Journal of Biomedicine and Biotechnology · doi:10.1155/2012/936486 · Cited by 824
The impact of oxidative stress and inflammation on RPE degeneration in non-neovascular AMD
Datta, S., Cano, M., Ebrahimi, K. B., Wang, L., & Handa, J. T. (2017) · Progress in Retinal and Eye Research · doi:10.1016/j.preteyeres.2017.03.002 · Cited by 843
Initiation and perpetuation of NLRP 3 inflammasome activation and assembly
Elliott, E. I., & Sutterwala, F. S. (2015) · Immunological Reviews · doi:10.1111/imr.12286 · Cited by 821
Glyburide inhibits the Cryopyrin/Nalp3 inflammasome
Lamkanfi, M., Mueller, J. L., Vitari, A. C., Misaghi, S., Fedorova, A., Deshayes, K., Lee, W. P., Hoffman, H. M., & Dixit, V. M. (2009) · Journal of Cell Biology · doi:10.1083/jcb.200903124 · Cited by 820
Autophagy Controls IL-1β Secretion by Targeting Pro-IL-1β for Degradation
Harris, J., Hartman, M., Roche, C., Zeng, S. G., O'Shea, A., Sharp, F. A., Lambe, E. M., Creagh, E. M., Golenbock, D. T., Tschopp, J., et al. (2011) · Journal of Biological Chemistry · doi:10.1074/jbc.m110.202911 · Cited by 794
Self-citationGold Nanoparticles of Diameter 1.4 nm Trigger Necrosis by Oxidative Stress and Mitochondrial Damage
Pan, Y., Leifert, A., Ruau, D., Neuß, S., Bornemann, J., Schmid, G., Brandau, W., Simon, U., & Jahnen‐Dechent, W. (2009) · Small · doi:10.1002/smll.200900466 · Cited by 802
Mitochondrial reactive oxygen species drive proinflammatory cytokine production
Naik, E., & Dixit, V. M. (2011) · Journal of Experimental Medicine · doi:10.1084/jem.20110367 · Cited by 783
The adaptor ASC has extracellular and 'prionoid' activities that propagate inflammation
Franklin, B. S., Bossaller, L., De Nardo, D., Ratter, J. M., Stutz, A., Engels, G., Brenker, C., Nordhoff, M., Mirandola, S. R., Al-Amoudi, A., et al. (2014) · Nature Immunology · doi:10.1038/ni.2913 · Cited by 773
The inflammasome: an integrated view
Gross, O., Thomas, C. J., Guarda, G., & Tschopp, J. (2011) · Immunological Reviews · doi:10.1111/j.1600-065x.2011.01046.x · Cited by 778
Self-citationNOD-Like Receptors: Role in Innate Immunity and Inflammatory Disease
Chen, G., Shaw, M. H., Kim, Y., & Núñez, G. (2008) · Annual Review of Pathology Mechanisms of Disease · doi:10.1146/annurev.pathol.4.110807.092239 · Cited by 796
The cell biology of inflammasomes: Mechanisms of inflammasome activation and regulation
Sharma, D., & Kanneganti, T. (2016) · The Journal of Cell Biology · doi:10.1083/jcb.201602089 · Cited by 754
Pattern Recognition Receptors and the Host Cell Death Molecular Machinery
Amarante-Mendes, G. P., Adjemian, S., Branco, L. M., Zanetti, L. C., Weinlich, R., & Bortoluci, K. R. (2018) · Frontiers in Immunology · doi:10.3389/fimmu.2018.02379 · Cited by 802
Synthetic Nanoparticles for Vaccines and Immunotherapy
Irvine, D. J., Hanson, M. C., Rakhra, K., & Tokatlian, T. (2015) · Chemical Reviews · doi:10.1021/acs.chemrev.5b00109 · Cited by 779
Mechanisms of Action of Adjuvants
Awate, S., Babiuk, L. A., & Mutwiri, G. (2013) · Frontiers in Immunology · doi:10.3389/fimmu.2013.00114 · Cited by 770
“Further, blocking ROS using chemical scavengers abolished NLRP3 activation in response to MSU suggesting a link between NLRP3 activation and ROS generation (Dostert et al., 2008).”
The role of oxidative stress during inflammatory processes
Lugrin, J., Rosenblatt‐Velin, N., Parapanov, R., & Liaudet, L. (2013) · Biological Chemistry · doi:10.1515/hsz-2013-0241 · Cited by 766
Abderrazak, A., Syrovets, T., Couchie, D., Hadri, K. E., Friguet, B., Simmet, T., & Rouis, M. (2015) · Redox Biology · doi:10.1016/j.redox.2015.01.008 · Cited by 749
Mechanisms of regulated unconventional protein secretion
Nickel, W., & Rabouille, C. (2008) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2617 · Cited by 726
Cao, X. (2015) · Nature reviews. Immunology · doi:10.1038/nri.2015.8 · Cited by 671
Inflammasome activation and IL-1β and IL-18 processing during infection
van de Veerdonk, F. L., Netea, M. G., Dinarello, C. A., & Joosten, L. A. B. (2011) · Trends in Immunology · doi:10.1016/j.it.2011.01.003 · Cited by 708
Necrotic cells trigger a sterile inflammatory response through the Nlrp3 inflammasome
Iyer, S. S., Pulskens, W. P., Sadler, J. J., Butter, L. M., Teske, G. J., Ulland, T. K., Eisenbarth, S. C., Florquin, S., Flavell, R. A., Leemans, J. C., et al. (2009) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0908698106 · Cited by 691
“S5A) 18 .”
Form Follows Function: Nanoparticle Shape and Its Implications for Nanomedicine
Kinnear, C., Moore, T. L., Rodríguez‐Lorenzo, L., Rothen‐Rutishauser, B., & Petri‐Fink, A. (2017) · Chemical Reviews · doi:10.1021/acs.chemrev.7b00194 · Cited by 685
NLRP3 Inflammasome and Inflammatory Bowel Disease
Yu, Z., & Zhang, H. (2019) · Frontiers in Immunology · doi:10.3389/fimmu.2019.00276 · Cited by 671
Sterile inflammation in the liver
Kubes, P., & Mehal, W. Z. (2012) · Gastroenterology · doi:10.1053/j.gastro.2012.09.008 · Cited by 666
Liu, J., Han, X., Zhang, T., Tian, K., Li, Z., & Luo, F. (2023) · Journal of Hematology & Oncology · doi:10.1186/s13045-023-01512-7 · Cited by 742
The role of IL-1β and TNF-α in intervertebral disc degeneration
Wang, Y., Che, M., Xin, J., Zheng, Z. J., Li, J., & Zhang, S. (2020) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2020.110660 · Cited by 634
Functions of ROS in Macrophages and Antimicrobial Immunity
Herb, M., & Schramm, M. (2021) · Antioxidants · doi:10.3390/antiox10020313 · Cited by 633
Walsh, J. G., Muruve, D. A., & Power, C. (2014) · Nature Reviews Neuroscience · doi:10.1038/nrn3638 · Cited by 637
Influenza virus activates inflammasomes via its intracellular M2 ion channel
Ichinohe, T., Pang, I. K., & Iwasaki, A. (2010) · Nature Immunology · doi:10.1038/ni.1861 · Cited by 632
“In addition, lysosomal membrane damage caused by phagocytosis of crystals such as asbestos, silica and aluminum salt triggers NLRP3 activatio”
Li, N., Zhou, H., Wu, H., Wu, Q., Duan, M., Deng, W., & Tang, Q. (2019) · Redox Biology · doi:10.1016/j.redox.2019.101215 · Cited by 595
Bauernfeind, F., Bartok, E., Rieger, A., Franchi, L., Núñez, G., & Hornung, V. (2011) · The Journal of Immunology · doi:10.4049/jimmunol.1100613 · Cited by 617
The signal pathways and treatment of cytokine storm in COVID-19
Yang, L., Xie, X., Tu, Z., Fu, J., Xu, D., & Zhou, Y. (2021) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-021-00679-0 · Cited by 618
Kool, M., Pétrilli, V., Smedt, T. D., Rolaz, A., Hammad, H., van Nimwegen, M., Bergen, I. M., Castillo, R., Lambrecht, B. N., & Tschopp, J. (2008) · The Journal of Immunology · doi:10.4049/jimmunol.181.6.3755 · Cited by 612
Self-citationSignaling by ROS drives inflammasome activation
Martinon, F. (2010) · European Journal of Immunology · doi:10.1002/eji.200940168 · Cited by 604
Zheng, M., & Kanneganti, T. (2020) · Immunological Reviews · doi:10.1111/imr.12909 · Cited by 602
Tetherin Inhibits HIV-1 Release by Directly Tethering Virions to Cells
Pérez-Caballero, D., Zang, T. M., Ebrahimi, A., McNatt, M. W., Gregory, D. A., Johnson, M. C., & Bieniasz, P. D. (2009) · Cell · doi:10.1016/j.cell.2009.08.039 · Cited by 590
The NLRP3 Inflammasome Promotes Renal Inflammation and Contributes to CKD
Vilaysane, A., Chun, J., Seamone, M. E., Wang, W., Chin, R., Hirota, S., Li, Y., Clark, S. A., Tschopp, J., Trpkov, K., et al. (2010) · Journal of the American Society of Nephrology · doi:10.1681/asn.2010020143 · Cited by 587
Self-citation
Metadata
- Authors
- Dostert, C., Pétrilli, V., Van Bruggen, R., Steele, C., Mossman, B. T., & Tschopp, J.
- Affiliations
- University of Vermont (US)
- Department of Biochemistry, University of Lausanne, Chemin des Boveresses 155, 1066 Epalinges, Switzerland.
- Venue
- Science
- Published
- 2008-05-02
- Volume
- 320
- Issue
- 5876
- Pages
- 674-677
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC2396588
- OpenAlex
- W2009004909
- Semantic Scholar
- d21a1e75f0ab181b382438ef2083584a4de9f54b
- Cited by
- 2,658
- References
- 27
- Citations by year
- 2026: 57 · 2025: 76 · 2024: 126 · 2023: 121 · 2022: 131 · 2021: 140 · 2020: 168 · 2019: 154 · 2018: 154 · 2017: 166 · 2016: 168 · 2015: 169 · 2014: 187 · 2013: 192 · 2012: 171
- FWCI
- 64.93
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- IRIS (submittedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Pure Amsterdam UMC (submittedVersion)
- SERVAL (Université de Lausanne) (submittedVersion, other-oa)
- Funders
- National Institutes of Health (5p01ca114047-05)
- National Heart, Lung, and Blood Institute (P01HL067004, P01 HL67004)
- National Cancer Institute (P01CA-114047)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Occupational and environmental lung diseases
- Keywords
- NLRP3 inflammasome, asbestos, silica, innate immune activation, IL-1β, reactive oxygen species, NADPH oxidase, phagocytosis, lung inflammation, pulmonary fibrosis, lung cancer, particulate matter
- MeSH terms
- NLR Family, Pyrin Domain-Containing 3 Protein, Animals, Asbestos, Carrier Proteins, Humans, Immunity, Inflammation, Macrophages, Silicon Dioxide, Inflammation Mediators, Mice, Interleukin-1beta
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-07, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-07 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
