Nanoparticles activate the NLR pyrin domain containing 3 (Nlrp3) inflammasome and cause pulmonary inflammation through release of IL-1α and IL-1β

Yazdi, Amir S.; Guarda, Greta; Riteau, Nicolas; Drexler, Stefan K.; Tardivel, Aubry; Couillin, Isabelle; Tschopp, Jürg

doi:10.1073/pnas.1008155107

Cited by 476 publications

(444 citation statements)

References 32 publications

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“…16,18 In general, long and fiber-shaped materials show higher acute cytotoxicity than their low aspect ratio counterparts. Moreover, the intracellular uptake of BNNTs observed by Ciofani and co-workers or seen in our study in apparently healthy cells (Figure 6c) may not lead to immediate (acute) cytotoxicity, but it may result in an inflammatory response, 20 aberrant mitosis, processes that in the long term may lead to tumorigenesis. The contradiction between the cytotoxicity studies of BNNTs could, at least in part, also be linked to the unconventional MTT assay employed by Ciofani and co-workers in the earlier studies.…”

supporting

confidence: 52%

In Vitro Investigation of the Cellular Toxicity of Boron Nitride Nanotubes

et al. 2011

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Nanotubes present one of the most promising opportunities in nanotechnology with a plethora of applications in nanoelectronics, mechanical engineering, as well as in biomedical technology. Due to their structure and some physical properties, boron nitride (BN) nanotubes (BNNTs) possess several advantages over carbon nanotubes (CNTs), and they are now commercially produced and used on a large scale. The human and environmental exposure to BN nanomaterials is expected to increase in the near future, and their biological responses need to be examined. Using complementary assays, we have extensively investigated the effects of BNNTs on the viability and metabolic status of different cell types: on the one hand, the effects on cells present in the lung alveoli, and on the other hand, on human embryonic kidney (HEK) cells. Our results indicate that BNNTs are cytotoxic for all cell types studied and, in most cases, are more cytotoxic than CNTs in their pristine (p-CNT) and functionalized (f-CNT) form. However, the level of toxicity and the prominent morphological alterations in the cell populations withstanding BNNT exposure are cell-type-dependent. For instance, BNNTs induced extensive multinucleated giant cell formation in macrophages and increased levels of eosinophilia in fibroblasts. Finally, our results point the toxicity of tubular nanomaterials to be strongly correlated with the cellular accumulation enhanced for straight nanotubes.

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confidence: 52%

In Vitro Investigation of the Cellular Toxicity of Boron Nitride Nanotubes

et al. 2011

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“…Even nanoparticles made from materials that are considered inert in bulk form have been found to induce pulmonary inflammation when exposure occurs with nanoscale particles. Although this study did not find TiO 2 nanoparticles to be inflammasome activating in macrophages, Yazdi et al (51) showed that in human keratinocytes nano-TiO 2 activates the NALP3 inflammasome and induces IL-1␤. Any or all of the potential mechanisms discussed may apply to the CB nanoparticle mechanism of inflammasome activation.…”

Section: Discussionmentioning

confidence: 88%

Induction of Inflammasome-dependent Pyroptosis by Carbon Black Nanoparticles

Reisetter

Stebounova

Baltrušaitis

et al. 2011

Journal of Biological Chemistry

167

103

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Inhalation of nanoparticles has been implicated in respiratory morbidity and mortality. In particular, carbon black nanoparticles are found in many different environmental exposures. Macrophages take up inhaled nanoparticles and respond via release of inflammatory mediators and in some cases cell death. Based on new data, we propose that exposure of macrophages (both a macrophage cell line and primary human alveolar macrophages) to carbon black nanoparticles induces pyroptosis, an inflammasome-dependent form of cell death. Exposure of macrophages to carbon black nanoparticles resulted in inflammasome activation as defined by cleavage of caspase 1 to its active form and downstream IL-1␤ release. The cell death that occurred with carbon black nanoparticle exposure was identified as pyroptosis by the protective effect of a caspase 1 inhibitor and a pyroptosis inhibitor. These data demonstrate that carbon black nanoparticle exposure activates caspase 1, increases IL-1␤ release after LPS priming, and induces the proinflammatory cell death, pyroptosis. The identification of pyroptosis as a cellular response to carbon nanoparticle exposure is novel and relates to environmental and health impacts of carbon-based particulates.Macrophages are critical regulators of local immune homeostasis. They are highly adaptive components of the innate immune system and respond in diverse ways to pathogens and other potential danger signals (1-3). In the lung, the alveolar macrophage is the first line of defense against environmental exposures. Alveolar macrophages phagocytose particulate matter, release inflammatory cytokines, and interact with other cells and molecules through the expression of surface receptors. One way in which an immune response is generated in alveolar macrophages is through the phagocytosis of deposited particles within the respiratory tract (4).The nanoparticle industry has expanded substantially in recent years. A variety of engineered carbon nanoparticles is used in consumer products such as car tires, rubber, and printer toner cartridges (5). Nanoparticles are also being used as novel means of drug delivery. Additionally, carbonaceous nanoparticles are present as an environmental contaminant. Combustion processes are a significant source of carbon nanoparticles. Elemental carbon-based nanoparticles with a diameter of less than 100 nm are a major part of diesel exhaust and ambient pollution (6).Particulate ambient pollution is known to cause adverse health effects in susceptible individuals and aggravates existing respiratory conditions such as asthma and chronic obstructive pulmonary disease (7). Even moderate levels of ambient air particulates are known to induce acute adverse health effects such as mortality in heart and lung diseases and chronic lung morbidity (8). Ultrafine particles are unique in their ability to bypass mucociliary clearance mechanisms and penetrate into deeper regions of the respiratory tract (9 -12). Although bulk elemental carbon is considered chemically inert (as in diamond and gra...

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“…Titania [ 16 ] and tripolyphosphate nanoparticles [ 17 ] have been shown to improve the biocompatibility of poly(lactic-co-glycolic acid) scaffolds, while nondegradable nanoparticles made of silica have been shown to induce infl ammation. [ 18 ] Infl ammatory cell interactions signifi cantly impact the biocompatibility and function of implanted scaffolds and can eventually cause their clinical failure [ 19 ] or success. For instance, local infl ammation is required to initiate the process of tissue regeneration and its control is considered necessary to guide the normal regeneration of damaged tissues.…”

Section: Introductionmentioning

confidence: 99%

In Vivo Host Response and Degradation of Copolymer Scaffolds Functionalized with Nanodiamonds and Bone Morphogenetic Protein 2

Suliman

Sun

Pedersen

et al. 2016

Adv Healthcare Materials

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The aim is to evaluate the effect of modifying poly[( L -lactide)-co-(ε-caprolactone)] scaffolds (PLCL) with nanodiamonds (nDP) or with nDP+physisorbed BMP-2 (nDP+BMP-2) on in vivo host tissue response and degradation. The scaffolds are implanted subcutaneously in Balb/c mice and retrieved after 1, 8, and 27 weeks. Molecular weight analysis shows that modifi ed scaffolds degrade faster than the unmodifi ed. Gene analysis at week 1 shows highest expression of proinfl ammatory markers around nDP scaffolds; although the presence of infl ammatory cells and foreign body giant cells is more prominent around the PLCL. Tissue regeneration markers are highly expressed in the nDP+BMP-2 scaffolds at week 8. A fi brous capsule is detectable by week 8, thinnest around nDP scaffolds and at week 27 thickest around PLCL scaffolds. mRNA levels of ALP, COL1α2, and ANGPT1 are signifi cantly upregulating in the nDP+BMP-2 scaffolds at week 1 with ectopic bone seen at week 8. Even when almost 90% of the scaffold is degraded at week 27, nDP are observable at implantation areas without adverse effects. In conclusion, modifying PLCL scaffolds with nDP does not aggravate the host response and physisorbed BMP-2 delivery attenuates infl ammation while lowering the dose of BMP-2 to a relatively safe and economical level.

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Nanoparticles activate the NLR pyrin domain containing 3 (Nlrp3) inflammasome and cause pulmonary inflammation through release of IL-1α and IL-1β

Cited by 476 publications

References 32 publications

In Vitro Investigation of the Cellular Toxicity of Boron Nitride Nanotubes

In Vitro Investigation of the Cellular Toxicity of Boron Nitride Nanotubes

Induction of Inflammasome-dependent Pyroptosis by Carbon Black Nanoparticles

In Vivo Host Response and Degradation of Copolymer Scaffolds Functionalized with Nanodiamonds and Bone Morphogenetic Protein 2

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