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.
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27 Own result · 24 Not checked yet · 9 Own interpretation
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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- 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
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
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
“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
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- 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
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- 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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- 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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- 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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- 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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- 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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- 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
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- 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
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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]
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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
boostedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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]
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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).
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