Cytokines asbestos

Geist EJ, Powers ES, Monick MM, et al. 2000. Asbestos stimulation triggers differential cytokine release from human monocytes and alveolar macrophages. Exp Fung Res 26 41-56. 

Hurbankova M, Kaiglova A. 1997. Some bronchoalveolar lavage parameters and leukocyte cytokine release in response to intratracheal instillation of short and long asbestos and wollastonite fibres in rats. Physiol Res 46 459-466. 

Ishihara Y, Kohyama N, Kagawa J. 1998. Contribution of human pulmonary macrophage-derived cytokines to asbestos-induced lung inflammation and fibrosis. Inhal Toxicol 10 205-225. 

Luster MI, Simeonova PP. 1998. Asbestos induces inflammatory cytokines in the lung through redox sensitive transcription factors. Toxicol Lett 102-103 271-275. 

Mongan LC, Jones T, Patrick G. 2000. Cytokine and free radical responses of alveolar macrophages in vitro to asbestos fibres. Cytokine 12(8) 1243-1247. 

Perkins RC, Scheule RK, Hamilton R, et al. 1993. Human alveolar macrophage cytokine release in response to in vitro and in vivo asbestos exposure. Exp Lung Res 19(l) 55-65. 

The first evidence indicating NF-tcB activation by asbestos was provided by Janssen et al. in 1995. In this study, they reported that crocidohte asbestos caused a dose-dependent increase in the binding of p50 and p65 proteirrs to NF-tcB-binding DNA elements in hamster tracheal epithelial (HTE) cells. Similarly, Simeonova and Luster showed that asbestos-induced NF-tcB activation is resporrsible for the increased expression of the inflammatory cytokine, lL-8, in htrman ptrlmorrary epithelial cells. ROS... 

Two interferon-Y-controUed metabolic pathways accounting for some of the cytostatic effects of interferon-y in rat pleural mesothelial cells transformed in vitro with benzo[a] pyrene or chrysotile asbestos were not efficient in human mesothelioma cells, and suggested that cytokine-induced growth inhibition is mediated by a different pathway in human mesothelioma cell lines (Phan-Bitch etal. 1997). 

Exposure to dusts such as silica and asbestos is associated with expression of various proinflammatory and fibrogenic cytokines, some of which (e.g., macrophage inflammatory protein-2 MIP-2) may be produced in epithelial cells (30), although most are probably produced in alveolar macrophages. Exposure of rats... 

Fibrosis of the walls of small airways and diffuse interstitial fibrosis are both associated with particle exposure. Several different mechanisms are probably operative. There is some evidence that exposure to asbestos and possibly other types of mineral particles causes increased permeability of the epithelium to small molecules (33) this process may allow particle-evoked, alveolar macrophage-derived growth factors and other cytokines to reach interstitial fibroblasts (30). The mechanism of increased permeability is disputed, with data extant that both support and deny a role for AOS (34,35). 

Mediators of both the infiammatoiy and fibrotic responses have been associated with exposure to oxidants. Similarly, mediator release after incubation of cells with silica and asbestos can be the result of oxygen-based free radicals catalyzed by iron associated with the mineral oxide (Fig. 1). The increase in arachidonic acid metabolism after exposures of cells to particles and fibers can result from the eooxidation of arachidonate by metal-catalyzed oxidants. This is a lipid peroxidation that can be mediated by free radical production by the dust (83). In support of an association between metal-catalyzed oxidant generation and arachidonic acid products, the release of LTB4 by alveolar macrophages can increase with the eoneentrations of iron complexed to the surface of silica and asbestos (84). Similarly, the eellular release of eytokines postulated to participate in the infiammatory and fibrotic responses ean be associated with exposures to metal-dependent radicals (see Fig. 1). TNF-a produetion by alveolar macrophages after mineral oxide exposure can be inhibited by both the metal chelator deferoxamine and hydroxyl radical scavengers (74). The release of other cytokines pertinent to silica and asbestos exposure ean also be responsive to oxidative stress (85,86). The release of these pertinent mediators after dust exposures is likely to be controlled by oxidant-sensitive promoters such as nuclear factor (NF)-kB (87). After exposure to silica and asbestos, NF-kB can function as a promoter... 

Figure 1 Schematic of an association between mediator release after silica and asbestos exposure and metal-catalyzed oxidant generation by the partieles Eieosanoid production can result from a co-oxidation of arachidonate by metal-catalyzed oxidants generated by the partieles. Similarly, the release of other cytokines pertinent to siliea and asbestos exposure can be responsive to oxidant-sensitive promoters.

Lemaire I, Beaudoin H, Dubois C. Cytokine regulation of lung fibroblast proliferation pulmonary and systemic changes in asbestos-induced pulmonary fibrosis. Am Rev Respir Dis 1986 134 653-658. 

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