Nickel Nanoparticles cause exaggerated lung and airway remodeling in mice lacking the T-box transcription factor, TBX21 (T-bet)

Glista-Baker, Ellen E.; Taylor, Alexia J.; Sayers, Brian C.; Thompson, Elizabeth A.; Bonner, James C.

doi:10.1186/1743-8977-11-7

Cited by 41 publications

(34 citation statements)

References 59 publications

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“…Additionally, this study also showed that the ability of several different types of MWCNTs to stimulate proliferation was correlated with prolonged ERK1/2 signaling specifically in fibroblasts 56 . Furthermore, rat pleural mesothelial cells treated in vitro with MWCNTs or nickel nanoparticles, a residual catalyst present in some MWCNTs, caused prolonged PDGF-induced ERK1/2 signaling and synergistically enhanced PDGF-induced chemokine production 97 . Mesothelial cell signaling of fibroblasts via chemokines or growth factors could be a mechanism of subpleural fibrosis observed in mice exposed to MWCNTs by inhalation 5 .…”

Section: Mechanisms Of Cnt-induced Fibrosismentioning

confidence: 97%

Mechanisms of carbon nanotube‐induced pulmonary fibrosis: a physicochemical characteristic perspective

Duke

Bonner

2017

WIREs Nanomed Nanobiotechnol

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Carbon nanotubes (CNTs) are engineered nanomaterials (ENMs) with numerous beneficial applications. However, they could pose a risk to human health from occupational or consumer exposures. Rodent models demonstrate that exposure to CNTs via inhalation, instillation, or aspiration results in pulmonary fibrosis. The severity of the fibrogenic response is determined by various physicochemical properties of the nanomaterial such as residual metal catalyst content, rigidity, length, aggregation status, or surface charge. CNTs are also increasingly functionalized post-synthesis with organic or inorganic agents to modify or enhance surface properties. The mechanisms of CNT-induced fibrosis involve oxidative stress, innate immune responses of macrophages, cytokine and growth factor production, epithelial cell injury and death, expansion of the pulmonary myofibroblast population, and consequent extracellular matrix accumulation. A comprehensive understanding of how physicochemical properties affect the fibrogenic potential of various types of CNTs should be considered in combination with genetic variability and gain or loss of function of specific genes encoding secreted cytokines, enzymes, or intracellular cell signaling molecules. Here, we cover the current state of the literature on mechanisms of CNT-exposed pulmonary fibrosis in rodent models with a focus on physicochemical characteristics as principal drivers of the mechanisms leading to pulmonary fibrosis. This article is categorized under: Therapeutic Approaches and Drug Discovery > Nanomedicine for Respiratory Disease Toxicology and Regulatory Issues in Nanomedicine > Toxicology of Nanomaterials.

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Section: Mechanisms Of Cnt-induced Fibrosismentioning

confidence: 97%

Mechanisms of carbon nanotube‐induced pulmonary fibrosis: a physicochemical characteristic perspective

Duke

Bonner

2017

WIREs Nanomed Nanobiotechnol

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“…However, the high demand for these materials, in concert with their toxicity potential, may pose a future health risk for humans. Pulmonary exposure studies in murine models have revealed that MWCNT exposure has negative consequences, including chronic inflammation leading to granuloma formation and fibrosis, along with asthma-like pathology (Glista-Baker et al, 2014; Hamilton et al, 2007, 2012, 2013; Mercer et al, 2011, 2013). The mechanisms that promote chronic inflammation are not clear, but activation of the NLRP3 inflammasome in macrophages and IL-1β signaling has been shown to be necessary for MWCNT-induced inflammation (Girtsman et al, 2012; Hamilton et al, 2012; Palomaki et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Extracellular HMGB1 regulates multi-walled carbon nanotube-induced inflammation in vivo

Jessop

Holian

2014

Nanotoxicology

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Endotoxin is often used to activate NF-κB in vitro when assessing NLRP3 inflammasome activation by various exogenous particles including nanoparticles. However, the endogenous source of this signal 1 is unknown. High-mobility group box 1 (HMGB1) is known to play a critical role in acute lung injury, however the potential contribution of the alarmin HMGB1 to NLRP3 Inflammasome activation has not been determined in response to nanoparticles in vivo. In this study, the ability of multi-walled carbon nanotubes (MWCNT) to cause release of HMGB1 in vitro and in vivo, as well as the potential of HMGB1 to function as signal 1 in vitro and in vivo, was determined. HMGB1 activity in vivo was assessed by administration of HMGB1 neutralization antibodies following MWCNT exposure. Caspase-1−/− mice were utilized to elucidate the dependence of HMGB1 secretion on NLRP3 inflammasome activity. MWCNT exposure increased extracellular HMGB1 levels in primary alveolar macrophages from C57Bl/6 mice and C10 mouse epithelial cell culture supernatants, and in C57Bl/6 mouse lung lavage fluid. MWCNT-induced HMGB1 secretion was dependent upon caspase-1. HMGB1 increased MWCNT-induced IL-1β release from macrophages in vitro, and neutralization of extracellular HMGB1 reduced MWCNT-induced IL-1β secretion in vivo. HMGB1 neutralization was accompanied with overall decreased inflammation. In summary, this study suggests extracellular HMGB1 participates in NLRP3 inflammasome activity and regulates IL-1β associated sterile inflammation induced by MWCNT.

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“…Additionally, concerning respiratory disorders, exposure to different types of NPs was able to exacerbate pre-existing inflammatory conditions of the respiratory tract, as reported in animal models of lipopolysaccharide-induced respiratory disease (Cesta et al, 2010; Inoue, 2011) or to aggravate allergen induced airway hyper-reactivity (Hussain et al, 2011; Inoue et al, 2009, 2010) as well as to exacerbate inflammation, mucous cell metaplasia and fibrosis in mice asthma (Glista-Baker et al, 2014; Ryman-Rasmussen et al, 2008) and cystic fibrosis models (Geiser et al, 2014). Taken together, NP exposure may synergistically facilitate pathological inflammatory conditions in the lung via both innate and adaptive immunological abnormalities.…”

Section: Resultsmentioning

confidence: 83%

Biomarkers of susceptibility: State of the art and implications for occupational exposure to engineered nanomaterials

Iavicoli

Leso

Schulte

2016

Toxicology and Applied Pharmacology

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Rapid advances and applications in nanotechnology are expected to result in increasing occupational exposure to nano-sized materials whose health impacts are still not completely understood. Scientific efforts are required to identify hazards from nanomaterials and define risks and precautionary management strategies for exposed workers. In this scenario, the definition of susceptible populations, which may be at increased risk of adverse effects may be important for risk assessment and management. The aim of this review is to critically examine available literature to provide a comprehensive overview on susceptibility aspects potentially affecting heterogeneous responses to nanomaterials workplace exposure. Genetic, genotoxic and epigenetic alterations induced by nanomaterials in experimental studies were assessed with respect to their possible function as determinants of susceptibility. Additionally, the role of host factors, i.e. age, gender, and pathological conditions, potentially affecting nanomaterial toxicokinetic and health impacts, were also analysed. Overall, this review provides useful information to obtain insights into the nanomaterial mode of action in order to identify potentially sensitive, specific susceptibility biomarkers to be validated in occupational settings and addressed in risk assessment processes. The findings of this review are also important to guide future research into a deeper characterization of nanomaterial susceptibility in order to define adequate risk communication strategies. Ultimately, identification and use of susceptibility factors in workplace settings has both scientific and ethical issues that need addressing.

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Nickel Nanoparticles cause exaggerated lung and airway remodeling in mice lacking the T-box transcription factor, TBX21 (T-bet)

Cited by 41 publications

References 59 publications

Mechanisms of carbon nanotube‐induced pulmonary fibrosis: a physicochemical characteristic perspective

Mechanisms of carbon nanotube‐induced pulmonary fibrosis: a physicochemical characteristic perspective

Extracellular HMGB1 regulates multi-walled carbon nanotube-induced inflammation in vivo

Biomarkers of susceptibility: State of the art and implications for occupational exposure to engineered nanomaterials

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