Environmentally relevant metal and transition metal ions enhance Fc epsilon RI-mediated mast cell activation.

Walczak‐Drzewiecka, Aurelia; Wyczółkowska, J; Dastych, Jarosław

doi:10.1289/ehp.5960

Cited by 28 publications

(13 citation statements)

References 54 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…It was reported that the metal components and transition metal from particles may be risk factors for respiratory symptoms. [30][31][32] Hong et al 1,5 reported that metal components (eg, Pb, Mn, and Fe) in particles might reduce daily mean PEFR of schoolchildren, a finding similar to ours. Also, we found that significant decrement of daily mean PEFR was associated with transition metals, including Ni, Fe, Mn, and Cr.…”

Section: Discussionsupporting

confidence: 87%

See 1 more Smart Citation

Effects of Airborne Metals on Lung Function in Inner Mongolian Schoolchildren

Madaniyazi

Lee

et al. 2013

Journal of Occupational &Amp; Environmental Medicine

View full text Add to dashboard Cite

show abstract

Section: Discussionsupporting

confidence: 87%

“…43 Evidence suggests that Fe may be responsible for the effect of particulates on the respiratory system. 31,44 Extra deposit of Fe through airborne particles could lead to increased oxidative damage. 40,45 Iron was associated with increased mortality 46,47 and stimulation of airway inflammation.…”

Section: Discussionmentioning

confidence: 99%

Effects of Airborne Metals on Lung Function in Inner Mongolian Schoolchildren

Madaniyazi

Lee

et al. 2013

Journal of Occupational &Amp; Environmental Medicine

View full text Add to dashboard Cite

show abstract

“…Similar results were observed for nickel (II) sulfate. 126 Both airway epithelial cells and alveolar macrophages may phagocytize irritant particles and as a result of the encounters, synthesize pro-inflammatory cytokines that induce airway inflammation and contribute to airway lesions in asthma and chronic obstructive pulmonary disorder. 127 Goto et al showed that in response to PM 10 particulate, alveolar macrophages released macrophage colony-stimulating factor (M-CSF), macrophage inflammatory protein-1ß, GM-CSF, IL-6, TNF-α, IL-1ß, IL-8, and monocyte chemotactic protein (MCP-1).…”

Section: Immune Cells and Metallo-particles: Mixed Immunological Actimentioning

confidence: 99%

Toxic elements in tobacco and in cigarette smoke: inflammation and sensitization

2011

View full text Add to dashboard Cite

Biochemically and pathologically, there is strong evidence for both atopic and nonatopic airway sensitization, hyperresponsiveness, and inflammation as a consequence of exposure to tobacco mainstream or sidestream smoke particulate. There is growing evidence for the relation between exposure to mainstream and sidestream smoke and diseases resulting from reactive oxidant challenge and inflammation directly as a consequence of the combined activity of neutrophils, macrophages, dendritic cells, eosinophils, basophils, as a humoral immunological consequence of sensitization, and that the metal components of the particulate play a role in adjuvant effects. As an end consequence, carcinogenicity is a known outcome of chronic inflammation.Smokeless tobacco has been evaluated by the IARC as a group 1 carcinogen. Of the many harmful constituents in smokeless tobacco, oral tissue metallothionein gradients suggest that metals contribute to the toxicity from smokeless tobacco use and possibly sensitization.This work reviews and examines work on probable contributions of toxic metals from tobacco and smoke to pathology observed as a consequence of smoking and the use of smokeless tobacco. Metals and metalloids in tobaccoThough exposure to substances from tobacco use is obviously a complex exposure, the carcinogens in tobacco smoke have been classified for health risk determinations into five major chemical classes. 1 Some of these have been carefully studied, contributing to a strong weight of evidence for associated health risks. 2 Toxic metals and metalloids constitute one of the more understudied major carcinogenic chemical classes in smokeless tobacco products and tobacco smoke. Eight of the top forty substances in the Fowles and Dybing table of cancer risk indices are metals or metalloid compounds. 1 In their table of non-cancer risk indices for individual chemical constituents of mainstream cigarette smoke based on a single cigarette per day, three of the top eight listed for respiratory effect health risk, cadmium, hexavalent chromium, and nickel, were metals. Another metalloid, silicon in the form of silicates, poses serious health risks by inhalation, but limited data is available, likely due to analytical difficulties.Metals and metalloids in smoke from biomass combustion including tobacco are generally considered to be present in ionic form, but may also occur in a gaseous elemental form, as is the case for mercury. 3 Whether a tobacco product is consumed by smoking or in a smokeless form, the exposure to toxic metals is directly related to the concentration in the tobacco leaf, assuming no metal containing additives are included during manufacture. [4][5][6] The soil (including any amendments to the soil such as sludge, fertilizers, or irrigation with

show abstract

“…Other environmental contaminants, such as certain heavy metals, have been reported to enhance Fc⑀RI-mediated mast cell degranulation, a mast cell response associated with allergic disease (31). Therefore, the ability of silica to alter IgE-dependent BMMC degranulation was assessed.…”

Section: W-shmentioning

confidence: 99%

Silica-Directed Mast Cell Activation Is Enhanced by Scavenger Receptors

Brown

Swindle

Kushnir-Sukhov

et al. 2007

Am J Respir Cell Mol Biol

View full text Add to dashboard Cite

Inhalation of crystalline silica results in pulmonary fibrosis and silicosis. It has been suggested that mast cells play a role in these conditions. How mast cells would influence pathology is unknown. We thus explored mast cell interactions with silica in vitro and in B6.CgKit W-sh mast cell-deficient mice. B6.Cg-Kit W-sh mice did not develop inflammation or significant collagen deposition after instillation of silica, while C57Bl/6 wild-type mice did have these findings. Given this supporting evidence of a role for mast cells in the development of silicosis, we examined the ability of silica to activate mouse bone marrow-derived mast cells (BMMC), including degranulation (␤-hexosaminidase release); production of reactive oxygen species (ROS) and inflammatory mediators; and the effects of silica on Fc⑀RI-dependent activation. Silica did not induce mast cell degranulation. However, TNF-␣, IL-13, monocyte chemotactic protein-1, protease activity, and production of ROS were dose-dependently increased after silica exposure, and production was enhanced after Fc⑀RI stimulation. This mast cell activation was inhibited by anti-inflammatory compounds. As silica mediates some effects in macrophages through scavenger receptors (SRs), we first determined that mast cells express scavenger receptors; then explored the involvement of SR-A and macrophage receptor with colleagenous structure (MARCO). Silica-induced ROS formation, apoptosis, and TNF-␣ production were reduced in BMMC obtained from SR-A, MARCO, and SR-A/MARCO knockout mice. These findings demonstrate that silica directs mast cell production of inflammatory mediators, in part through SRs, providing insight into critical events in the pathogenesis and potential therapeutic targets in silicosis. Keywords: B6.Cg-kitW-sh sash mouse; CD204; macrophage receptor with collagenous structure; mast cell; silicosis; SR-A Among environmental exposures that lead to pathologic changes in tissues is crystalline silica, which can result in occupational silicosis from inhalation of silica dusts in manufacturing, construction, farming, and mining operations. Silicosis, for which there is no effective treatment, leads to decreased pulmonary function and increased susceptibility to diseases of the respiratory tract (1, 2).Involvement of mast cells in silica-induced pulmonary inflammation has been suggested by two clinical observations. First, the number of mast cells within the lungs of individuals exposed to silica dust is increased (3). Second, an increase in mast cells staining for basic fibroblast growth factor located within silicotic nodules has been reported in lung sections obtained from patients with silicosis (4). Despite the suggestive CLINICAL RELEVANCEThis study demonstrates a role for mast cells in silicosis and is the first study to examine direct effects of silica on mast cell biology. It provides evidence that treatment of silicosis should explore mast cells as a potential therapeutic target.evidence for a role of mast cells in the development of silicosis, there are ...

show abstract

Environmentally relevant metal and transition metal ions enhance Fc epsilon RI-mediated mast cell activation.

Cited by 28 publications

References 54 publications

Effects of Airborne Metals on Lung Function in Inner Mongolian Schoolchildren

Effects of Airborne Metals on Lung Function in Inner Mongolian Schoolchildren

Toxic elements in tobacco and in cigarette smoke: inflammation and sensitization

Silica-Directed Mast Cell Activation Is Enhanced by Scavenger Receptors

Contact Info

Product

Resources

About