silica/vefjadrep

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Pre-exposure of Mycobacterium tuberculosis-infected macrophages to crystalline silica impairs control of bacterial growth by deregulating the balance between apoptosis and necrosis.

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Inhalation of crystalline silica (CS) particles increases the risk of pulmonary tuberculosis; however, the precise mechanism through which CS exposure facilitates Mycobacterium tuberculosis (Mtb) infection is unclear. We speculate that macrophage exposure to CS deregulates the cell death pathways

Silica increases tumor necrosis factor (TNF) production, in part, by upregulating the TNF promoter.

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Silica causes release of tumor necrosis factor (TNF) from mononuclear phagocytes. One hypothesis is that silica increases TNF production, in part, by upregulating the TNF gene. To evaluate this hypothesis, THP-1 cells (a myelomonocytic cell line) were exposed to various amounts of silica and then

[Involvement of Toll-like receptor in silica-induced tumor necrosis factor alpha release from human macrophage cell line].

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OBJECTIVE To characterize the role of Toll-like receptor 4 (TLR4) in silica-induced production of tumor necrosis factor alpha (TNFalpha) from macrophage cell line. METHODS The human macrophage cell line THP-1 was incubated with silica suspension. Cell media were collected and TNFalpha levels in the

Resistance to silica-induced lung fibrosis in senescent rats: role of alveolar macrophages and tumor necrosis factor-alpha (TNF).

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The purpose of the present study was to investigate the effect of aging on silica-induced lung toxicity. In young animals silica induced a significant increase in bronchoalveolar lavage tumor necrosis factor-alpha (TNF), lactate dehydrogenase as well as in cell numbers, which correlate with

Fluoroimmunoassay for tumor necrosis factor-alpha in human serum using Ru(bpy)(3)Cl(2)-doped fluorescent silica nanoparticles as labels.

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A novel fluoroimmunoassay (FIA) method was developed for the determination of tumor necrosis factor-alpha (TNF-alpha) in this study. The proposed method has the advantage of showing the specificity of immunoassays and sensitivity of fluorescent nanoparticles label technology. With the

Dose-dependent cell necrosis induced by silica nanoparticles.

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In recent years, much attention has been given to nanoparticles (NPs) due to their many possible applications, and as research has progressed, these NPs have become valuable tools for medical purposes. Among many different types of NPs, silica nanoparticles (SiO₂NPs) have been

Peritoneal lavage fluids stimulate NIH3T3 fibroblast proliferation and contain increased tumour necrosis factor and IL-6 in experimental silica-induced rat peritonitis.

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Fibroblast proliferation is one of the earliest features of fibrosis, preceding collagen deposition in wound. The response to tissue injury is characterized by the infiltration of acute inflammatory cells, followed by persistence of macrophages. In vitro, macrophages are known to secrete monokines

Antisense inhibition of silica-induced tumor necrosis factor in alveolar macrophages.

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Tumor necrosis factor-alpha (TNFalpha) has been shown to play an important role in the pathogenesis of silicotic fibrosis. In this study, antisense oligonucleotides targeted to TNFalpha mRNA were used to inhibit silica-induced TNFalpha gene expression in alveolar macrophages. To achieve

Asbestos fibers and silica particles stimulate rat alveolar macrophages to release tumor necrosis factor. Autoregulatory role of leukotriene B4.

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Alveolar macrophages (AM) can play a crucial role in the pathogenesis of pulmonary disease via their ability to produce potent inflammatory and fibrogenic mediators. We found that rat AM cultured with 1 to 100 micrograms/ml of silica particles or asbestos fibers produced tumor necrosis factor (TNF)

[Effects of taurine on tumor necrosis factor expression of lung in rats treated by silica].

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OBJECTIVE To evaluate the effects of taurine on the expression of tumor necrosis factor-alpha (TNF-alpha) protein of lung in rats treated by silica. METHODS 144 Wistar rats were randomly divided into three experimental groups: saline-instilled with a control diet (saline-treated group),

Sensitive immunoassay of a biomarker tumor necrosis factor-alpha based on poly(guanine)-functionalized silica nanoparticle label.

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A novel electrochemical immunosensor for the detection of tumor necrosis factor-alpha (TNF-alpha) based on poly(guanine)-functionalized silica nanoparticles (NPs) label is presented. The detection of mouse TNF-alpha via immunological reaction is based on a dual signal amplification: (1) a large

Phosphorylation of tumor necrosis factor receptor 1 (p55) protects macrophages from silica-induced apoptosis.

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Macrophages play a fundamental role in silicosis in part by removing silica particles and producing inflammatory mediators in response to silica. Tumor necrosis factor alpha (TNFalpha) is a prominent mediator in silicosis. Silica induction of apoptosis in macrophages might be mediated by TNFalpha.

Silica-induced apoptosis in murine macrophage: involvement of tumor necrosis factor-alpha and nuclear factor-kappaB activation.

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Alveolar macrophages play a critical role in silica-induced lung fibrosis. Silica exposure induces tumor necrosis factor (TNF)-alpha release and nuclear factor (NF)-kappaB activation, and apoptotic mechanisms have been implicated in silica-induced pathogenesis. To characterize potential

Requirement of tumour necrosis factor for development of silica-induced pulmonary fibrosis.

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The deposition of silica particles in the lung of man or experimental animals leads to silicosis, a disease of progressive respiratory failure caused by a fibrotic reaction. It has long been suspected that the phagocytosis of silica by pulmonary macrophages induces the secretion of fibrogenic

Soluble tumor necrosis factor (TNF) receptors p55 and p75 and interleukin-10 downregulate TNF-alpha activity during the lung response to silica particles in NMRI mice.

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We have found reduced activity of tumor necrosis factor (TNF)-alpha accompanying resolving and fibrosing alveolitis induced in NMRI mice by mineral particles (MnO2 and SiO2, respectively), which is in apparent contradiction to the well-recognized proinflammatory and profibrotic activities of this

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