Influence of silica particles on mucociliary structure and MUC5B expression in airways of C57BL/6 mice

Yu, Qimei; Fu, Guoqing; Lin, Hui; Zhao, Qianqian; Liu, Yuewei; Zhou, Yun; Shi, Yuqin; Zhang, Ling; Wang, Zhenyu; Zhang, Zhibing; Qin, Lingzhi; Zhou, Ting

doi:10.1080/01902148.2020.1762804

Cited by 11 publications

(10 citation statements)

References 35 publications

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“…Using the human airway epithelial cells 16HBE or primary cultured mouse tracheobronchial epithelial cells, researchers found that SiO 2 nanoparticles could inhibit the responses to ATP and inhibit cation channel transient receptor potential vanilloid 4 (TRPV4) in airway epithelial cells, and result in epithelial barrier dysfunction (46,47). In vitro and in vivo experiments demonstrated that SiO 2 particles exposure not only caused rapid NLRP3-dependent mitochondrial depolarization and DNA damage in airway epithelial cells but also led to ultrastructural defects in airway cilia and mucus hypersecretion (48,49). Besides, one review concluded that SiO 2 particles might bind to the scavenger receptor of alveolar macrophages, followed by particle endocytosis with a respiratory burst to generate reactive oxygen species and reactive nitrogen species, which in turn activation of the protein kinase C mediated MAPK signaling cascades resulting in cytokine release (50).…”

Section: Discussionmentioning

confidence: 99%

Nano-silica particles synergistically IgE-mediated mast cell activation exacerbating allergic inflammation in mice

et al. 2022

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BackgroundAllergic respiratory diseases have increased dramatically due to air pollution over the past few decades. However, studies are limited on the effects of inorganic components and particulate matter with different particle sizes in smog on allergic diseases, and the possible molecular mechanism of inducing allergies has not been thoroughly studied.MethodsFour common mineral elements with different particle sizes in smog particles were selected, including Al2O3, TiO2, Fe2O3, and SiO2. We studied the relationship and molecular mechanism of smog particle composition, particle size, and allergic reactions using mast cells, immunoglobulin E (IgE)-mediated passive cutaneous anaphylaxis (PCA) model, and an ovalbumin (OVA)-induced asthmatic mouse model in vitro and in vivo, combined with transmission electron microscopy, scanning transmission X-ray microscopy analysis, and transcriptome sequencing.ResultsOnly 20 nm SiO2 particles significantly increased β-hexosaminidase release, based on dinitrophenol (DNP)-human serum albumin (HSA) stimulation, from IgE-sensitized mast cells, while other particles did not. Meanwhile, the PCA model showed that Evan’s blue extravasation in mice was increased after treatment with nano-SiO2 particles. Nano-SiO2 particles exposure in the asthmatic mouse model caused an enhancement of allergic airway inflammation as manifested by OVA-specific serum IgE, airway hyperresponsiveness, lung inflammation injury, mucous cell metaplasia, cytokine expression, mast cell activation, and histamine secretion, which were significantly increased. Nano-SiO2 particles exposure did not affect the expression of FcϵRI or the ability of mast cells to bind IgE but synergistically activated mast cells by enhancing the mitogen-activated protein kinase (MAPK) signaling pathway, especially the phosphorylation levels of the extracellular signal-regulated kinase (ERK)1/2. The ERK inhibitors showed a significant inhibitory effect in reducing β-hexosaminidase release.ConclusionOur results indicated that nano-SiO2 particles stimulation might synergistically activate IgE-sensitized mast cells by enhancing the MAPK signaling pathway and that nano-SiO2 particles exposure could exacerbate allergic inflammation. Our experimental results provide useful information for preventing and treating allergic diseases.

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Section: Discussionmentioning

confidence: 99%

Nano-silica particles synergistically IgE-mediated mast cell activation exacerbating allergic inflammation in mice

et al. 2022

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“…Tracheal epithelium is not only a mechanical barrier to external stimuli and microbes, but also actively involved in innate and acquired immune responses during tracheal inflammation [ 29 ]. Constantly exposed to viruses, bacteria, or dust particles, the tracheal barrier structure will be destroyed, and the immune cells which then be activated by secreting a variety of cytokines and chemokines, thereby promoting the occurrence of tracheal injury [ 30 ]. Thus, tracheal epithelial cells have been speculated to be a key regulator of tracheal pathophysiology in various tracheal injury-related respiratory diseases, such as allergic asthma, chronic obstructive pulmonary disease, and cystic fibrosis [ 31 ].…”

Section: Discussionmentioning

confidence: 99%

Ferulic acid ameliorates lipopolysaccharide-induced tracheal injury via cGMP/PKGII signaling pathway

Xie

Hou

et al. 2021

Respir Res

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Background Tracheal injury is a common clinical condition that still lacks an effective therapy at present. Stimulation of epithelial sodium channel (ENaC) increases Na+ transport, which is a driving force to keep tracheal mucosa free edema fluid during tracheal injury. Ferulic acid (FA) has been proved to be effective in many respiratory diseases through exerting anti-oxidant, anti-inflammatory, and anti-thrombotic effects. However, these studies rarely involve the level of ion transport, especially ENaC. Methods C57BL/J male mice were treated intraperitoneally with normal saline or FA (100 mg/kg) 12 h before, and 12 h after intratracheal administration of lipopolysaccharide (LPS, 5 mg/kg), respectively. The effects of FA on tracheal injury were not only assessed through HE staining, immunofluorescence assay, and protein/mRNA expressions of ENaC located on tracheas, but also evaluated by the function of ENaC in mouse tracheal epithelial cells (MTECs). Besides, to explore the detailed mechanism about FA involved in LPS-induced tracheal injury, the content of cyclic guanosine monophosphate (cGMP) was measured, and Rp-cGMP (cGMP inhibitor) or cGMP-dependent protein kinase II (PKGII)-siRNA (siPKGII) were applied in primary MTECs, respectively. Results Histological examination results demonstrated that tracheal injury was obviously attenuated by pretreatment of FA. Meanwhile, FA could reverse LPS-induced reduction of both protein/mRNA expressions and ENaC activity. ELISA assay verified cGMP content was increased by FA, and administration of Rp-cGMP or transfection of siPKGII could reverse the FA up-regulated ENaC protein expression in MTECs. Conclusions Ferulic acid can attenuate LPS-induced tracheal injury through up-regulation of ENaC at least partially via the cGMP/PKGII pathway, which may provide a promising new direction for preventive and therapeutic strategy in tracheal injury.

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“…In addition to causing direct injury, dust particles may also lead to a reduction in mucociliary clearance. Yu et al demonstrated that silica particles impaired mucociliary clearance by causing ultrastructural defects in airway cilia, overproduction of mucus, and alteration of MUC5B expression in the trachea [ 79 ]. As a result, toxic particles cannot be removed from the lungs by phagocytosis or mucociliary clearance, leading to continuous exposure to dust particles.…”

Section: Pathogenic Mechanisms Of Dental Dustmentioning

confidence: 99%

Characterization of dental dust particles and their pathogenicity to respiratory system: a narrative review

Ding

et al. 2023

Clin Oral Invest

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Objectives Dental professionals are exposed to large amounts of dust particles during routine treatment and denture processing. This article provides a narrative review to investigate the most prevalent dust-related respiratory diseases among dental professionals and to discuss the effects of dental dust on human respiratory health. Materials and methods A literature search was performed in PubMed/Medline, Web of Science, and Embase for articles published between 1990 and 2022. Any articles on the occupational respiratory health effects of dental dust were included. Results The characterization and toxicity evaluation of dental dust show a correlation between dust exposure and respiratory system injury, and the possible pathogenic mechanism of dust is to cause lung injury and abnormal repair processes. The combination use of personal protective equipment and particle removal devices can effectively reduce the adverse health effects of dust exposure. Conclusions Dental dust should be considered an additional occupational hazard in dental practice. However, clinical data and scientific evidence on this topic are still scarce. Further research is required to quantify dust in the dental work environment and clarify its pathogenicity and potential toxicological pathways. Nonetheless, the prevention of dust exposure should become a consensus among dental practitioners. Clinical relevance This review provides dental practitioners with a comprehensive understanding and preventive advice on respiratory health problems associated with dust exposure.

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Influence of silica particles on mucociliary structure and MUC5B expression in airways of C57BL/6 mice

Cited by 11 publications

References 35 publications

Nano-silica particles synergistically IgE-mediated mast cell activation exacerbating allergic inflammation in mice

Nano-silica particles synergistically IgE-mediated mast cell activation exacerbating allergic inflammation in mice

Ferulic acid ameliorates lipopolysaccharide-induced tracheal injury via cGMP/PKGII signaling pathway

Characterization of dental dust particles and their pathogenicity to respiratory system: a narrative review

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