ArticleEnvironmental health perspectives1997
Asbestos and silica-induced changes in human alveolar macrophage phenotype.
Article in Environmental health perspectives, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 53 citations in OpenAlex.
- Nested case-control study of autoimmune disease in an asbestos-exposed population.Environmental health perspectives · 2006Trial
- Differences in Cytokine Expression at Baseline and in Response to Mineral Stimulation by Peripheral Blood Mononuclear Cells from Podoconiosis Cases and Healthy Control Individuals.Tropical medicine and infectious disease · 2024Article
- The effect of feed supplementation with Transcarpathian zeolite (clinoptilolite) on the concentrations of acute phase proteins and cytokines in the serum and hepatic tissue of chickens.Poultry science · 2020Article
- The Secretory Response of Rat Peritoneal Mast Cells on Exposure to Mineral Fibers.International journal of environmental research and public health · 2018Article
- STB-HO, a novel mica fine particle, inhibits the teratoma-forming ability of human embryonic stem cells after in vivo transplantation.Oncotarget · 2016Article
- Mica Nanoparticle, STB-HO Eliminates the Human Breast Carcinoma Cells by Regulating the Interaction of Tumor with its Immune Microenvironment.Scientific reports · 2015Article
- Modulation of macrophage activities in proliferation, lysosome, and phagosome by the nonspecific immunostimulator, mica.PloS one · 2015Article
- Article
- Supplementation of dietary germanium biotite enhances induction of the immune responses by foot-and-mouth disease vaccine in cattle.BMC veterinary research · 2014Article
- Erionite induces production of autoantibodies and IL-17 in C57BL/6 mice.Toxicology and applied pharmacology · 2014Article
- Autoimmunity and asbestos exposure.Autoimmune diseases · 2014Review
- Alteration of fibroblast phenotype by asbestos-induced autoantibodies.Journal of immunotoxicology · 2011Article
- Nonpulmonary outcomes of asbestos exposure.Journal of toxicology and environmental health. Part B, Critical reviews · 2011Review
- Assessing the in vitro toxicity of the lunar dust environment using respiratory cells exposed to Al(2)O(3) or SiO(2) fine dust particles.In vitro cellular & developmental biology. Animal · 2009Article
- Silica binding and toxicity in alveolar macrophages.Free radical biology & medicine · 2008Review
- Assessment of autoimmune responses associated with asbestos exposure in Libby, Montana, USA.Environmental health perspectives · 2005Article
- Flow cytometry in the exploration of the physiopathology of occupational lung disease.Occupational and environmental medicine · 1999Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The mechanism by which fibrogenic particulates induce inflammation that can progress to lung fibrosis is uncertain. The alveolar macrophage (AM) has been implicated in the inflammatory process because of its function and reported release of inflammatory mediators when isolated from fibrotic patients. It has been recently shown that fibrogenic, but not nonfibrogenic, particulates are highly potent in inducing apoptosis of human AM. In this study, we tested the hypothesis that fibrogenic particulates could shift the phenotypic ratio of human AM to a more inflammatory condition. The macrophage phenotypes were characterized by flow cytometry targeting the RFD1 and RFD7 epitopes. Results demonstrated that chrysotile and crocidolite asbestos, as well as crystalline silica, but not titanium dioxide or wollastonite, increased the RFD1+ phenotype (inducer or immune activator macrophages) and decreased the RFD1+ RFD7+ phenotype (suppressor macrophages). These results provide a mechanistic explanation that may link apoptosis (namely, suppressor macrophages) to a shift in the ratio of macrophage phenotypes that could initiate lung inflammation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.