Double-walled carbon nanotubes trigger IL-1β release in human monocytes through Nlrp3 inflammasome activation

Meunier, Étienne; Coste, Agnès; Olagnier, David; Authier, Hélène; Lefèvre, Lise; Dardenne, Christophe; Bernad, José; Béraud, Maryse; Flahaut, Emmanuel; Pipy, Bernard

doi:10.1016/j.nano.2011.11.004

Cited by 119 publications

(89 citation statements)

References 32 publications

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“…Activation of the NLRP3 inflammasome in macrophages, in addition to IL-1β signaling, has been shown to be necessary for CNT-induced inflammation. 17,18 Moreover, Nlrp3-deficient mice have been shown to exhibit reduced pulmonary inflammation and inflammatory cytokine production following exposure to asbestos compared with wild-type mice. 19 Ni 2+ contamination of multi-walled CNTs is related to particle bioactivity and is correlated with NLRP3 inflammasome activation.…”

Section: Introductionmentioning

confidence: 99%

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Exposure to nickel oxide nanoparticles induces pulmonary inflammation through NLRP3 inflammasome activation in rats

Cao¹,

Fang²,

Lu³

et al. 2016

IJN

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With recent advances in the manufacture and application of nickel oxide nanoparticles (NiONPs), concerns about their adverse effects on the respiratory system are increasing. However, the underlying cellular and molecular mechanisms of NiONP-induced pulmonary toxicity remain unclear. In this study, we focused on the impacts of NiONPs on pulmonary inflammation and investigated whether the NLRP3 inflammasome is involved in NiONP-induced pulmonary inflammation and injury. NiONP suspensions were administered by single intratracheal instillation to rats, and inflammatory responses were evaluated at 3 days, 7 days, or 28 days after treatment. NiONP exposure resulted in sustained pulmonary inflammation accompanied by inflammatory cell infiltration, alveolar proteinosis, and cytokine secretion. Expression of Nlrp3 was markedly upregulated by the NiONPs, which was accompanied by overexpression of the active form of caspase-1 (p20) and interleukin (IL)-1β secretion in vivo. NiONP-induced IL-1β secretion was partially prevented by co-treatment with a caspase-1 inhibitor in macrophages. Moreover, siRNA-mediated Nlrp3 knockdown completely attenuated NiONP-induced cytokine release and caspase-1 activity in macrophages in vitro. In addition, NiONP-induced NLRP3 inflammasome activation requires particle uptake and reactive oxygen species production. Collectively, our findings suggest that the NLRP3 inflammasome participates in NiONP-induced pulmonary inflammation and offer new strategies to combat the pulmonary toxicity induced by NiONPs.

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Section: Introductionmentioning

confidence: 99%

“…Accumulating evidences indicate that NPs trigger an inflammation and toxicity following endocytosis into the target cells. 47 Meunier et al 17 showed that phagocytosis of fibrous particles is required as an initial step for inflammasome activation. The actin cytoskeleton plays a vital role in phagocytizing long materials or particles.…”

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confidence: 99%

Exposure to nickel oxide nanoparticles induces pulmonary inflammation through NLRP3 inflammasome activation in rats

Cao¹,

Fang²,

Lu³

et al. 2016

IJN

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“…Air pollution containing carbon nanoparticles, environmental air contaminants that might be easily inhaled with C. pneumoniae, also appears to be a critical factor in the pathogenesis of asthma (9-11). Recent studies indicated that carbon black or carbon nanotubes (CNTs), belonging to carbon nanoparticles, stimulate IL-1␤ secretion from lipopolysaccharide (LPS)-primed macrophages (12)(13)(14).IL-1␤ secretion is strictly controlled by two different steps: (i) pro-IL-1␤ transcription and (ii) the cleavage of pro-IL-1␤ by a caspase-1-containing protein complex, the inflammasome (15-17). First, pro-IL-1␤ is transcribed via NF-B activation following signaling from pattern recognition receptors (PRRs), such as Tolllike receptors (TLRs) (signal 1).…”

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confidence: 99%

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confidence: 99%

Synergistic Costimulatory Effect of Chlamydia pneumoniae with Carbon Nanoparticles on NLRP3 Inflammasome-Mediated Interleukin-1β Secretion in Macrophages

et al. 2015

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The obligate intracellular bacterium Chlamydia pneumoniae is not only a causative agent of community-acquired pneumonia but is also associated with a more serious chronic disease, asthma, which might be exacerbated by air pollution containing carbon nanoparticles. Although a detailed mechanism of exacerbation remains unknown, the proinflammatory cytokine interleukin-1␤ (IL-1␤) is a critical player in the pathogenesis of asthma. C. pneumoniae induces IL-1␤ in macrophages via NACHT, LRR, and PYD domain-containing protein 3 (NLRP3) inflammasome activation and Toll-like receptor 2/4 (TLR2/4) stimulation. Carbon nanoparticles, such as carbon nanotubes (CNTs), can also evoke the NLRP3 inflammasome to trigger IL-1␤ secretion from lipopolysaccharide-primed macrophages. This study assessed whether costimulation of C. pneumoniae with CNTs synergistically enhanced IL-1␤ secretion from macrophages, and determined the molecular mechanism involved. Enhanced IL-1␤ secretion from C. pneumoniae-infected macrophages by CNTs was dose and time dependent. Transmission electron microscopy revealed that C. pneumoniae and CNTs were engulfed concurrently by macrophages. Inhibitors of actin polymerization or caspase-1, a component of the inflammasome, significantly blocked IL-1␤ secretion. Gene silencing using small interfering RNA (siRNA) targeting the NLRP3 gene also abolished IL-1␤ secretion. Other inhibitors (K ؉ efflux inhibitor, cathepsin B inhibitor, and reactive oxygen species-generating inhibitor) also blocked IL-1␤ secretion. Taken together, these findings demonstrated that CNTs synergistically enhanced IL-1␤ secretion from C. pneumoniae-infected macrophages via the NLRP3 inflammasome and caspase-1 activation, providing novel insight into our understanding of how C. pneumoniae infection can exacerbate asthma. Chlamydia pneumoniae is an obligate intracellular bacterium and a causative agent of respiratory tract infections, including community-acquired pneumonia (1, 2). The seroprevalence rates of C. pneumoniae infection, which start to rise relatively early in childhood, are increased by 50% at 20 years of age and subsequently reach 70 to 80% by 60 to 70 years of age (3, 4), suggesting most individuals will have had some exposure to the bacterium in their lifetime. Therefore, C. pneumoniae is likely a ubiquitous pathogen in individuals worldwide (4). The symptoms of pulmonary infection vary considerably according to age from asymptomatic or mild illness to serious pneumonia, especially in pediatric infection (1-3). Regarding this, several studies indicate that bacterial infection might exacerbate pulmonary inflammation and thus is associated with a more serious chronic disease, asthma (3). The proinflammatory cytokine interleukin-1␤ (IL-1␤), which is induced by C. pneumoniae (5-8), is thought to play a critical role in the development of chronic inflammatory disease, although detailed mechanisms remain unclear. Air pollution containing carbon nanoparticles, environmental air contaminants that might be easily inhaled with C. pneu...

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“…Furthermore, recent reports have suggested that it is not only the size but also the shape that determines the extent of the toxicity (Bhattacharjee et al, 2012). Long fibers, such as asbestos and CNTs, are known to be phagocytosed by lung macrophages and dendritic cells, which may result in IL-1β secretion and inflammatory cell death through NLRP3 inflammasomes (Goodglick and Kane, 1986;Dostert et al, 2008;Meunier et al, 2012;Kanno et al, 2015). It has also been verified that agglomerates over a particular length threshold induce 'frustrated phagocytosis' (Murphy et al, 2012;Schinwald and Donaldson, 2012).…”

Section: Discussionmentioning

confidence: 99%

Phagocytosis-dependent and independent mechanisms underlie the microglial cell damage caused by carbon nanotube agglomerates

Shigemoto-Mogami¹,

Hoshikawa²,

Hirose

et al. 2016

J. Toxicol. Sci.

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-Although carbon nanotubes (CNTs) are used in many fields, including energy, healthcare, environmental technology, materials, and electronics, the adverse effects of CNTs in the brain are poorly understood. In this study, we investigated the effects of CNTs on cultured microglia, as microglia are the first responders to foreign materials. We compared the effects of sonicated suspensions of 5 kinds of CNTs and their flow-through filtered with a 0.22 μm membrane filter on microglial viability. We found that sonicated suspensions caused microglial cell damage, but their flow-through did not. The number of microglial aggregates was well correlated with the extent of the damage. We also determined that the CNT agglomerates consisted of two groups: one was phagocytosed by microglia and caused microglial cell damage, and the other caused cell damage without phagocytosis. These results suggest that phagocytosis-dependent and independent mechanisms underlie the microglial cell damage caused by CNT agglomerates and it is important to conduct studies about the relationships between physical properties of nanomaterial-agglomerates and cell damage.

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Double-walled carbon nanotubes trigger IL-1β release in human monocytes through Nlrp3 inflammasome activation

Cited by 119 publications

References 32 publications

Exposure to nickel oxide nanoparticles induces pulmonary inflammation through NLRP3 inflammasome activation in rats

Exposure to nickel oxide nanoparticles induces pulmonary inflammation through NLRP3 inflammasome activation in rats

Synergistic Costimulatory Effect of Chlamydia pneumoniae with Carbon Nanoparticles on NLRP3 Inflammasome-Mediated Interleukin-1β Secretion in Macrophages

Phagocytosis-dependent and independent mechanisms underlie the microglial cell damage caused by carbon nanotube agglomerates

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