Role of Scavenger Receptor A Family in Lung Inflammation from Exposure to Environmental Particles

Department of Biomedical and Pharmaceutical Sciences, Center for Environmental Health Sciences, University of Montana, Missoula, Montana 59812, USA.
Journal of Immunotoxicology (Impact Factor: 2.05). 05/2008; 5(2):151-7. DOI: 10.1080/15476910802085863
Source: PubMed


Both immune and non-immune cells express an extensive array of scavenger receptors that bind a variety of ligands including bacterial cell-wall components and lipoproteins. Over the past several years, significant advances have been made in elucidating the role of scavenger receptors, predominantly Class A scavenger receptors SR-A I/II and MARCO, on macrophages in the binding of environmental particles such as crystalline silica and titanium dioxide. Recent evidence indicates that the binding of crystalline silica to scavenger receptors leads to apoptosis of macrophages and release of mediators (e.g., proinflammatory cytokines) contributing to lung inflammation and fibrosis. In this review, we examine the evidence for the role of SR-A I/II and MARCO in binding of the environmental particles and signaling initiated by particle-receptor interaction. Emerging concepts on the molecular details of signaling cascades by engagement of scavenger receptors by the environmental particles are also discussed.

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    • "It is generally accepted that, like bacteria and viruses, particulate matter such as Asian dust particles is eliminated from the human body by phagocytes such as macrophages [16, 17]. Macrophages ingesting exogenous materials produce interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) and, through the activation of signal pathways such as the mitogen-activated protein kinase (MAPK) pathways, expedite the elimination of particulate matter by inducing inflammatory responses; however, excessive or chronic macrophage activation results in inflammatory diseases such as bronchitis or pneumonia [18]. "
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    ABSTRACT: Asian dust is a springtime meteorological phenomenon that originates in the deserts of China and Mongolia. The dust is carried by prevailing winds across East Asia where it causes serious health problems. Most of the information available on the impact of Asian dust on human health is based on epidemiological investigations, so from a biological standpoint little is known of its effects. To clarify the effects of Asian dust on human health, it is essential to assess inflammatory responses to the dust and to evaluate the involvement of these responses in the pathogenesis or aggravation of disease. Here, we investigated the induction of inflammatory responses by Asian dust particles in macrophages. Treatment with Asian dust particles induced greater production of inflammatory cytokines interleukin-6 and tumor necrosis factor- α (TNF- α ) compared with treatment with soil dust. Furthermore, a soil dust sample containing only particles ≤10 μ m in diameter provoked a greater inflammatory response than soil dust samples containing particles >10 μ m. In addition, Asian dust particles-induced TNF- α production was dependent on endocytosis, the production of reactive oxygen species, and the activation of nuclear factor- κ B and mitogen-activated protein kinases. Together, these results suggest that Asian dust particles induce inflammatory disease through the activation of macrophages.
    Research Journal of Immunology 05/2014; 2014(4464):856154. DOI:10.1155/2014/856154
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    • "MWCNTs had been found to induce apoptosis in vitro by activating caspase-3/7 (Sohaebuddin et al., 2010). It is also found that the interaction between large negative charged particles and scavenger receptors on alveolar macrophage (AM) might be involved in AM apoptosis (Iyer et al., 1996; Iyer and Holian, 1997; Holian et al., 1998; Obot et al., 2002; Thakur et al., 2008). Scavenger receptors on AM are involved "
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    ABSTRACT: We have demonstrated previously that the acid-treated multi-walled carbon nanotubes (aci-MWCNTs) and taurine functionalized MWCNTs (tau-MWCNTs) induced differential pulmonary toxicity in mice after instillation exposure. In order to compare differences of cytotoxicity between the aci- and tau-MWCNTs, RAW 264.7 cells (a murine macrophage cell line) were chosen to be exposed to the aci- and tau-MWCNTs at concentrations of 0, 5, 20, 40, and 80μg/ml for 12 or 24h respectively. The results showed that although the aci- and tau-MWCNTs induced only mild decrease in cell viability to RAW 264.7 cells, the two types of MWCNTs elicited significant increase in apoptosis and decreased ability in cellular phagocytosis. Moreover, by using the specific inhibitors, we found that the scavenger receptors (SR) and caspase-9 were actively involved in the apoptosis induced by the aci- and tau-MWCNTs. The taurine functionalized MWCNTs (tau-MWCNTs) showed less cytotoxicity and apoptotic effect to RAW 264.7 cells than those of aci-MWCNTs. Taken together, the results indicated the important role of scavenger receptors and mitochondria in the apoptosis induced by MWCNTs.
    Toxicology in Vitro 06/2012; 26(6):799-806. DOI:10.1016/j.tiv.2012.05.010 · 2.90 Impact Factor
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    • "(9) Transfer of silica particles and (partially cleaved) asbestos fibers to regional lymph nodes. (10) As these cellular and molecular reactions are continuously repeated, pulmonary fibrosis will appear gradually and progressively [48, 49]. "
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    ABSTRACT: Asbestos causes lung fibrosis known as asbestosis as well as cancers such as malignant mesothelioma and lung cancer. Asbestos is a mineral silicate containing iron, magnesium, and calcium with a core of SiO(2). The immunological effect of silica, SiO(2), involves the dysregulation of autoimmunity because of the complications of autoimmune diseases found in silicosis. Asbestos can therefore cause alteration of immunocompetent cells to result in a decline of tumor immunity. Additionally, due to its physical characteristics, asbestos fibers remain in the lung, regional lymph nodes, and the pleural cavity, particularly at the opening sites of lymphatic vessels. Asbestos can induce chronic inflammation in these areas due to the production of reactive oxygen/nitrogen species. As a consequence, immunocompetent cells can have their cellular and molecular features altered by chronic and recurrent encounters with asbestos fibers, and there may be modification by the surrounding inflammation, all of which eventually lead to decreased tumor immunity. In this paper, the brief results of our investigation regarding reduction of tumor immunity of immunocompetent cells exposed to asbestos in vitro are discussed, as are our findings concerned with an investigation of chronic inflammation and analyses of peripheral blood samples derived from patients with pleural plaque and mesothelioma that have been exposed to asbestos.
    BioMed Research International 02/2012; 2012:492608. DOI:10.1155/2012/492608 · 2.71 Impact Factor
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