Macrophages participate in local and systemic inflammation induced by amorphous silica nanoparticles through intratracheal instillation

Yang, Man; Li, Jing; Ji, Wang; Yu, Yang; Cao, Lige; Zhang, Lianshuang; Zhou, Xianqing; Sun, Zhiwei

doi:10.2147/ijn.s116492

Cited by 46 publications

(21 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…A large body of evidence has been gathered to suggest that SiO 2 -NP exposure induces inflammatory response in the lung. [26][27][28][29][30] We demonstrate here that the exposure of neonatal mice to SiO 2 -NPs led to macrophages internalizing the NPs and inflammatory cell infiltration. Microglia cells are regarded as macrophage-like cells that reside in the central nervous system (CNS) to mediate initial inflammation in the CNS.…”

Section: Discussionmentioning

confidence: 57%

Silica nanoparticle exposure during the neonatal period impairs hippocampal precursor proliferation and social behavior later in life

Gao

Gong

et al. 2018

IJN

View full text Add to dashboard Cite

IntroductionSilica nanoparticles (SiO2-NPs) are currently among the most widely used nanomaterials, but their potentially adverse effects on brain development remain unknown. The developing brain is extremely sensitive to NP neurotoxicity during the early postnatal period.Materials and methodsHerein, we investigated the effects of SiO2-NPs (doses of 10, 20, or 50 mg with a particle size of ~91 nm, equivalent to aerosol mass concentrations 55.56, 111.11, and 277.78 mg/m3, respectively) exposure from postnatal day (P) 1 to P7 on hippocampal precursor proliferation at P8 and long-term neurobehavior in adults.ResultsSiO2-NP exposure resulted in inflammatory cell infiltration in lung tissue, microglia over-activation in the hippocampal dentate gyrus (DG), and decreased hippocampal precursor proliferation in the DG-subgranular zone at P8. Moreover, after exposure to 20 mg of SiO2-NPs, mice exhibited social interaction deficits and slight anxiety-like behaviors in adulthood, but this exposure did not induce locomotor activity impairment, depression-like behavior, or short-term memory impairment.DiscussionThese findings suggest that early-age SiO2-NP exposure induced inflammation and inhibited precursor proliferation in the DG in a dose-dependent manner, which might be related to the social dysfunction observed in adulthood.

show abstract

Section: Discussionmentioning

confidence: 57%

Silica nanoparticle exposure during the neonatal period impairs hippocampal precursor proliferation and social behavior later in life

Gao

Gong

et al. 2018

IJN

View full text Add to dashboard Cite

show abstract

“…An example is given by pyrogenic amorphous silica that, contrary to other types of amorphous silica (e.g., Stöber silica, a colloidal silica), can induce lung inflammation (30) and increase collagen deposition after repeated dose administration in mice (35). Other studies showed that some Stöber silicas can cause inflammation in rodents (36,37), and it is possible to vary the toxicity of pyrogenic silica by adjusting the synthesis conditions (31). The identification of the origin of this variability would represent a significant advance for developing rational production and use of safer silica materials.…”

Section: Significancementioning

confidence: 99%

Nearly free surface silanols are the critical molecular moieties that initiate the toxicity of silica particles

Pavan

Santalucia

Leinardi

et al. 2020

Proc. Natl. Acad. Sci. U.S.A.

121

View full text Add to dashboard Cite

Inhalation of silica particles can induce inflammatory lung reactions that lead to silicosis and/or lung cancer when the particles are biopersistent. This toxic activity of silica dusts is extremely variable depending on their source and preparation methods. The exact molecular moiety that explains and predicts this variable toxicity of silica remains elusive. Here, we have identified a unique subfamily of silanols as the major determinant of silica particle toxicity. This population of “nearly free silanols” (NFS) appears on the surface of quartz particles upon fracture and can be modulated by thermal treatments. Density functional theory calculations indicates that NFS locate at an intersilanol distance of 4.00 to 6.00 Å and form weak mutual interactions. Thus, NFS could act as an energetically favorable moiety at the surface of silica for establishing interactions with cell membrane components to initiate toxicity. With ad hoc prepared model quartz particles enriched or depleted in NFS, we demonstrate that NFS drive toxicity, including membranolysis, in vitro proinflammatory activity, and lung inflammation. The toxic activity of NFS is confirmed with pyrogenic and vitreous amorphous silica particles, and industrial quartz samples with noncontrolled surfaces. Our results identify the missing key molecular moieties of the silica surface that initiate interactions with cell membranes, leading to pathological outcomes. NFS may explain other important interfacial processes involving silica particles.

show abstract

“…There is also evidence to support causative association of exposure to SiNPs with pulmonary fibrosis in animal models [5,6]. Besides, amorphous and crystal silica have been defined by the International Agency for Research on Cancer (IARC) as group 3 (inadequate evidence for carcinogenicity) and group 1 (sufficient evidence for the carcinogenicity to experimental animals and to humans) materials, respectively [7]. Thus, it is important to evaluate pulmonary inflammation induced by exposure to NPs, especially SiNPs, and better understand the underlying mechanisms.…”

Section: Introductionmentioning

confidence: 99%

Silica nanoparticles induce lung inflammation in mice via ROS/PARP/TRPM2 signaling-mediated lysosome impairment and autophagy dysfunction

et al. 2020

View full text Add to dashboard Cite

Background: Wide applications of nanoparticles (NPs) have raised increasing concerns about safety to humans. Oxidative stress and inflammation are extensively investigated as mechanisms for NPs-induced toxicity. Autophagy and lysosomal dysfunction are emerging molecular mechanisms. Inhalation is one of the main pathways of exposing humans to NPs, which has been reported to induce severe pulmonary inflammation. However, the underlying mechanisms and, more specifically, the interplays of above-mentioned mechanisms in NPs-induced pulmonary inflammation are still largely obscure. Considered that NPs exposure in modern society is often unavoidable, it is highly desirable to develop effective strategies that could help to prevent nanomaterials-induced pulmonary inflammation. Results: Pulmonary inflammation induced by intratracheal instillation of silica nanoparticles (SiNPs) in C57BL/6 mice was prevented by PJ34, a poly (ADP-ribose) polymerase (PARP) inhibitor. In human lung bronchial epithelial (BEAS-2B) cells, exposure to SiNPs reduced cell viability, and induced ROS generation, impairment in lysosome function and autophagic flux. Inhibition of ROS generation, PARP and TRPM2 channel suppressed SiNPs-induced lysosome impairment and autophagy dysfunction and consequent inflammatory responses. Consistently, SiNPs-induced pulmonary inflammation was prevented in TRPM2 deficient mice.

show abstract

Macrophages participate in local and systemic inflammation induced by amorphous silica nanoparticles through intratracheal instillation

Cited by 46 publications

References 28 publications

Silica nanoparticle exposure during the neonatal period impairs hippocampal precursor proliferation and social behavior later in life

Silica nanoparticle exposure during the neonatal period impairs hippocampal precursor proliferation and social behavior later in life

Nearly free surface silanols are the critical molecular moieties that initiate the toxicity of silica particles

Silica nanoparticles induce lung inflammation in mice via ROS/PARP/TRPM2 signaling-mediated lysosome impairment and autophagy dysfunction

Contact Info

Product

Resources

About