Cytokine and Free Radical Responses of Alveolar Macrophages in Vitro to Asbestos Fibres

Mongan, L.C.; Jones, T; Patrick, G.

doi:10.1006/cyto.2000.0700

Cited by 25 publications

(21 citation statements)

References 14 publications

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“…Asbestos is a fibrous mineral composed of silica used as an insulating material in hundreds of products (Mongan et al, 2000; Table 2). There are two types of asbestos fibers called serpentine and amphiboles asbestos.…”

Section: Asbestosismentioning

confidence: 99%

Environmental, Inhaled and Ingested Causes of Pulmonary Fibrosis

et al. 2007

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Pulmonary fibrosis is a general term that refers to a collection of connective tissue around alveolar structures. There are over 200 disorders where the lungs may be involved in a fibrotic response. To determine the cause of pulmonary fibrosis requires an in depth understanding of the pathogenesis of pulmonary fibrosis and breadth of knowledge of the causative agents and associated disorders that may lead to pulmonary fibrosis. A comprehensive evaluation of the patient is absolutely essential, starting with detailed history that includes an occupational and environmental history because fibrogenic exposures can occur in many settings. Equally important is a history of ingestion of pharmaceutical or nonpharmaceutical substances. A physical examination and judicious investigations are always a part of any comprehensive clinical assessment but they are not commonly helpful in elucidating the cause of most pulmonary fibrotic disorders. Although, a chest film is invariably done, a logical and strongly recommended next step is a high-resolution computed tomography (HRCT). HRCT provides a better assessment of the radiological pattern, may suggest a diagnosis as well as direct the site, and type of lung biopsy. If the history and investigations do not lead to a diagnosis then a lung biopsy is required. Prevention or removal of the inciting agent is critical to the treatment of these disorders and in some instances corticosteroids may be of help.

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Section: Asbestosismentioning

confidence: 99%

Environmental, Inhaled and Ingested Causes of Pulmonary Fibrosis

et al. 2007

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“…However, overproduction of pro-inflammatory cytokines and inflammatory molecules by activated macrophages is critical to the onset of inflammation 3 . In the presence of stimuli such as lipopolysaccharides (LPS), activated macrophages produce various cytokines such as tumour necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), and interleukin-10 (IL-10), and inflammatory mediators such as nitric oxide (NO) and prostaglandin E2 (PGE2) [4][5][6] . In our study, LPS was therefore used to activate macrophages to evaluate the anti-inflammatory effects of the leaf extract.…”

Section: Introductionmentioning

confidence: 99%

Anti-inflammatory effect of Morinda citrifolia leaf extract on macrophage RAW 264.7 cells

Saraphanchotiwitthaya

Sripalakit²

2015

ScienceAsia

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Leaves of Morinda citrifolia (Rubiaceae) have been used in folk medicine to treat pain and inflammation. In this study, the anti-inflammatory activity of M. citrifolia leaf extracts was investigated. The extract was prepared by freeze-drying juice squeezed from M. citrifolia leaves. HPLC analysis of the crude extract revealed rutin to be a major compound together with small amounts of quercetin and kaempferol. The effect of this extract on TNF-α, IL-1β, and NO secretion by lipopolysaccharide-induced macrophage RAW 264.7 cells was investigated and compared to that of rutin, dexamethasone, and indomethacin. The results show that the extract inhibited TNF-α (98%, 750 µg/ml) secretion four times more than dexamethasone (3.92 µg/ml) and indomethacin (3.58 µg/ml), while rutin had no effect. The extract suppressed IL-1β secretion in a dose-dependent fashion with a maximum inhibition of about 79% (750 µg/ml). This was similar to that achieved by dexamethasone (97%, 3.92 µg/ml), indomethacin (70%, 3.58 µg/ml), and rutin (90%, 48.84 µg/ml). Moreover, the extract inhibited NO secretion (74%, 750 µg/ml) 50% more than rutin (40 µM) and 70% more than dexamethasone and indomethacin (10 µM). This study demonstrates the potential of M. citrifolia leaves as an effective therapeutic intervention against inflammatory diseases.

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“…Macrophages play an important role in this process by releasing mutagenic reactive oxygen species (ROS) and cytokines that support inflammation (5)(6)(7)(8)(9). Among these cytokines, TNF-α has been identified as a critical mediator of the pathogenesis of asbestos-related disease.…”

mentioning

confidence: 99%

Programmed necrosis induced by asbestos in human mesothelial cells causes high-mobility group box 1 protein release and resultant inflammation

Yang

Rivera

Jube

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

237

255

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Asbestos carcinogenesis has been linked to the release of cytokines and mutagenic reactive oxygen species (ROS) from inflammatory cells. Asbestos is cytotoxic to human mesothelial cells (HM), which appears counterintuitive for a carcinogen. We show that asbestos-induced HM cell death is a regulated form of necrosis that links to carcinogenesis. Asbestos-exposed HM activate poly(ADP-ribose) polymerase, secrete H 2 O 2 , deplete ATP, and translocate high-mobility group box 1 protein (HMGB1) from the nucleus to the cytoplasm, and into the extracellular space. The release of HMGB1 induces macrophages to secrete TNF-α, which protects HM from asbestos-induced cell death and triggers a chronic inflammatory response; both favor HM transformation. In both mice and hamsters injected with asbestos, HMGB1 was specifically detected in the nuclei, cytoplasm, and extracellular space of mesothelial and inflammatory cells around asbestos deposits. TNF-α was coexpressed in the same areas. HMGB1 levels in asbestos-exposed individuals were significantly higher than in nonexposed controls (P < 0.0001). Our findings identify the release of HMGB1 as a critical initial step in the pathogenesis of asbestos-related disease, and provide mechanistic links between asbestos-induced cell death, chronic inflammation, and carcinogenesis. Chemopreventive approaches aimed at inhibiting the chronic inflammatory response, and especially blocking HMGB1, may decrease the risk of malignant mesothelioma among asbestos-exposed cohorts.mesothelioma | tumor necrosis factor-alpha | carcinogenesis | biomarker | chemoprevention

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Cytokine and Free Radical Responses of Alveolar Macrophages in Vitro to Asbestos Fibres

Cited by 25 publications

References 14 publications

Environmental, Inhaled and Ingested Causes of Pulmonary Fibrosis

Environmental, Inhaled and Ingested Causes of Pulmonary Fibrosis

Anti-inflammatory effect of Morinda citrifolia leaf extract on macrophage RAW 264.7 cells

Programmed necrosis induced by asbestos in human mesothelial cells causes high-mobility group box 1 protein release and resultant inflammation

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