Silver nanoparticles induce apoptosis through the Toll-like receptor 2 pathway

Kim, An-Sook; Chae, Chang-Hoon; Kim, Juliana; Choi, Je‐Yong; Kim, Seong‐Gon; Băciuț, Grigore

doi:10.1016/j.oooo.2012.01.019

Cited by 24 publications

(20 citation statements)

References 35 publications

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“…A causative mechanism of NF‐κB expression is ROS, which can lead to several inflammatory responses including mitochondrial DNA release, causing NLRP3 inflammasome activation (Hehner et al ., ; Gloire et al ., ; Shimada et al ., ). AgNP entry into cells is believed to occur via receptor‐mediated endocytosis, and evidence suggests that AgNP can activate toll‐like receptor pathways, another mechanism of NF‐κB activation (Kim et al ., , ). It is possible that TLR‐2 is involved as it has been demonstrated that AgNP‐induced apoptosis can be partially mediated by the TLR‐2 signaling pathway (Kim et al ., ; Dubey et al ., ).…”

Section: Discussionmentioning

confidence: 99%

“…AgNP entry into cells is believed to occur via receptor‐mediated endocytosis, and evidence suggests that AgNP can activate toll‐like receptor pathways, another mechanism of NF‐κB activation (Kim et al ., , ). It is possible that TLR‐2 is involved as it has been demonstrated that AgNP‐induced apoptosis can be partially mediated by the TLR‐2 signaling pathway (Kim et al ., ; Dubey et al ., ). Interaction of AgNP with a TLR coupled with AgNP induction of NF‐κB highlights a possible mechanism for inflammasome activation.…”

Section: Discussionmentioning

confidence: 99%

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Silver nanoparticles induce pro‐inflammatory gene expression and inflammasome activation in human monocytes

Murphy¹,

Casey²,

Byrne

et al. 2016

J of Applied Toxicology

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A complete cytotoxic profile of exposure to silver (AgNP) nanoparticles investigating their biological effects on the innate immune response of circulating white blood cells is required to form a complete understanding of the risk posed. This was explored by measuring AgNP-stimulated gene expression of the pro-inflammatory cytokines interleukin-1 (IL-1), interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-α) in THP-1 monocytes. A further study, on human monocytes extracted from a cohort of blood samples, was carried out to compare with the AgNP immune response in THP-1 cells along with the detection of pro-IL-1β which is a key mediator of the inflammasome complex.The aims of the study were to clearly demonstrate that AgNP can significantly up-regulate pro-inflammatory cytokine gene expression of IL-1, IL-6 and TNF-α in both THP-1 cells and primary blood monocytes thus indicating a rapid response to AgNP in circulation. Furthermore, a role for the inflammasome in AgNP response was indicated by pro-IL-1β cleavage and release. These results highlight the potential inflammatory effects of AgNP exposure and the responses evoked should be considered with respect to the potential harm that exposure may cause.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Silver nanoparticles induce pro‐inflammatory gene expression and inflammasome activation in human monocytes

Murphy¹,

Casey²,

Byrne

et al. 2016

J of Applied Toxicology

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“…One explanation for the size dependence could be that the smaller nanoparticles produce more hydrogen peroxide than the larger ones [60]. Silver nanoparticles may induce dosedependent effects on different cell types in terms of both cytotoxicity and TLR2 expression [61]. Silver nanoparticle-induced apoptosis is reduced after treatment with TLR2 siRNA [61].…”

Section: Nanoparticlesmentioning

confidence: 99%

“…Silver nanoparticles may induce dosedependent effects on different cell types in terms of both cytotoxicity and TLR2 expression [61]. Silver nanoparticle-induced apoptosis is reduced after treatment with TLR2 siRNA [61]. Functional blocking of TLR2 with anti-TLR2 antibodies inhibits silver nanoparticle-mediated cytotoxicity [61].…”

Section: Nanoparticlesmentioning

confidence: 99%

Role of the Toll Like Receptor (TLR) Radical Cycle in Chronic Inflammation: Possible Treatments Targeting the TLR4 Pathway

Lucas¹,

2013

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Activation of the Toll-like receptor 4 (TLR4) complex, a receptor of the innate immune system, may underpin the pathophysiology of many human diseases, including asthma, cardiovascular disorder, diabetes, obesity, metabolic syndrome, autoimmune disorders, neuroinflammatory disorders, schizophrenia, bipolar disorder, autism, clinical depression, chronic fatigue syndrome, alcohol abuse, and toluene inhalation. TLRs are pattern recognition receptors that recognize damage-associated molecular patterns and pathogen-associated molecular patterns, including lipopolysaccharide (LPS) from gram-negative bacteria. Here we focus on the environmental factors, which are known to trigger TLR4, e.g., ozone, atmosphere particulate matter, long-lived reactive oxygen intermediate, pentachlorophenol, ionizing radiation, and toluene. Activation of the TLR4 pathways may cause chronic inflammation and increased production of reactive oxygen and nitrogen species (ROS/RNS) and oxidative and nitrosative stress and therefore TLR-related diseases. This implies that drugs or substances that modify these pathways may prevent or improve the abovementioned diseases. Here we review some of the most promising drugs and agents that have the potential to attenuate TLR-mediated inflammation, e.g., anti-LPS strategies that aim to neutralize LPS (synthetic anti-LPS peptides and recombinant factor C) and TLR4/MyD88 antagonists, including eritoran, CyP, EM-163, epigallocatechin-3-gallate, 6-shogaol, cinnamon extract, N-acetylcysteine, melatonin, and molecular hydrogen. The authors posit that activation of the TLR radical (ROS/RNS) cycle is a common pathway underpinning many "civilization" disorders and that targeting the TLR radical cycle may be an effective method to treat many inflammatory disorders.

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“…It is worth mentioning that targeted inhibition of TLR-2 substantially reduced nanoparticle mediated cell death (Kim et al, 2012). Silver nanoparticles have also been shown to strongly induce apoptosis in murine dendritic cell line in a ROS dependent manner (Kang et al, 2012).…”

Section: Silver Nanoparticlesmentioning

confidence: 99%

Nanoparticle Induced Oxidative Stress in Cancer Cells: Adding New Pieces to an Incomplete Jigsaw Puzzle

Nogueira¹,

Rolim²,

Farooqı³

2014

Asian Pacific Journal of Cancer Prevention

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Nanotechnology is an emerging field with many promising applications in drug delivery systems. Because of outstanding developments in this field, rapidly increasing research is directed to the development of nanocarriers that may enhance the availability of drugs to the target sites. Substantial fraction of information has been added into the existing scientific literature focusing on the fact that nanoparticles usually generate reactive oxygen species to a greater extent than micro-sized particles. It is worth mentioning that oxidative stress regulates an array of cell signaling cascades that resulted in cancer cell damage. Accumulating experimental evidence over the years has shown that wide-ranging biological mechanisms are triggered by these NPs in cultured cells due to the unique properties of engineered nanoparticles. In this review, we have attempted to provide an overview of the signaling cascades that are activated by oxidative stress in cancer cells in response to different kinds of nanomaterials, including quantum dots, metallic and polymeric nanoparticles.

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Silver nanoparticles induce apoptosis through the Toll-like receptor 2 pathway

Cited by 24 publications

References 35 publications

Silver nanoparticles induce pro‐inflammatory gene expression and inflammasome activation in human monocytes

Silver nanoparticles induce pro‐inflammatory gene expression and inflammasome activation in human monocytes

Role of the Toll Like Receptor (TLR) Radical Cycle in Chronic Inflammation: Possible Treatments Targeting the TLR4 Pathway

Nanoparticle Induced Oxidative Stress in Cancer Cells: Adding New Pieces to an Incomplete Jigsaw Puzzle

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