Pulmonary Response to Silica or Titanium Dioxide: Inflammatory Cells, Alveolar Macrophage-derived Cytokines, and Histopathology

Driscoll, Kevin E.; Lindenschmidt, Robert C.; Maurer, James K.; Higgins, Janet; Ridder, Gregg

doi:10.1165/ajrcmb/2.4.381

Cited by 230 publications

(121 citation statements)

References 31 publications

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“…Among the cytokines secreted following phagocytosis of silica particles, TNF-␣ has been shown to play a critical role in the pathogenesis of silicosis (15,42), and actions that antagonize the biological effects of TNF-␣ ameliorate silica-induced fibrosis in mice (46,47). TNF-␣ may also be necessary for the expression of other more downstream growth factors and the consequent development of fibrosis (54,55).…”

Section: Discussionmentioning

confidence: 99%

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Scavenger receptor class A type I/II (CD204) null mice fail to develop fibrosis following silica exposure

Beamer¹,

Holian²

2005

American Journal of Physiology-Lung Cellular and Molecular Phys

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Alveolar macrophages express the class A scavenger receptor (CD204) (Babaev VR, Gleaves LA, Carter KJ, Suzuki H, Kodama T, Fazio S, and Linton MF. Arterioscler Thromb Vasc Biol 20: 2593–2599, 2000); yet its role in vivo in lung defense against environmental particles has not been clearly defined. In the current study, CD204 null mice (129Sv background) were used to investigate the link between CD204 and downstream events of inflammation and fibrosis following silica exposure in vivo. CD204−/− macrophages were shown to recognize and uptake silica in vitro, although this response was attenuated compared with 129Sv wild-type mice. The production of tumor necrosis factor-α in lavage fluid was significantly enhanced in CD204 null mice compared with wild-type mice following silica exposure. Moreover, after exposure to environmental particles, CD204−/− macrophages exhibited improved cell viability in a dose-dependent manner compared with wild-type macrophages. Finally, histopathology from a murine model of chronic silicosis in 129Sv wild-type mice displayed typical focal lesions, interstitial thickening with increased connective tissue matrix, and cellular infiltrate into air space. In contrast, CD204−/− mice exhibited little to no deposition of collagen, yet they demonstrated enhanced accumulation of inflammatory cells largely composed of neutrophils. Our findings point to an important role of CD204 in mounting an efficient and appropriately regulated immune response against inhaled particles. Furthermore, these results indicate that the functions of CD204 are critical to the development of fibrosis and the resolution of inflammation.

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Section: Discussionmentioning

confidence: 99%

“…In the lung, the alveolar macrophage (AM) is primarily responsible for the binding, ingestion, and clearance of inhaled particulate matter (15). The AM response to inhaled particulates ranges from ingestion and clearance with minimal inflammation to profuse production of inflammatory cytokines and reactive oxygen intermediates (1,10,61).…”

mentioning

confidence: 99%

Scavenger receptor class A type I/II (CD204) null mice fail to develop fibrosis following silica exposure

Beamer¹,

Holian²

2005

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…the dose and type of silica used and the mode of silica instillation. With regard to the dose, Driscoll et al (1) showed that silica stimulation of TNF␣ release occurred only at doses greater than 50 mg/kg. Lemaire (26) also reported the lack of silica effect on TNF␣ release at a low silica dose of 15 mg/kg.…”

Section: Figmentioning

confidence: 99%

“…Tumor necrosis factor-␣ (TNF␣) 1 is a macrophage-derived peptide that has been shown to play an important role in the pathogenesis of pulmonary fibrosis (1)(2)(3). Several fibrogenic agents such as crystalline silica and asbestos stimulate TNF␣ mRNA expression and protein synthesis in macrophages (2,3).…”

mentioning

confidence: 99%

Antisense Inhibition of Silica-induced Tumor Necrosis Factor in Alveolar Macrophages

Rojanasakul¹,

Weissman

Shi

et al. 1997

Journal of Biological Chemistry

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Tumor necrosis factor-␣ (TNF␣) has been shown to play an important role in the pathogenesis of silicotic fibrosis. In this study, antisense oligonucleotides targeted to TNF␣ mRNA were used to inhibit silica-induced TNF␣ gene expression in alveolar macrophages. To achieve macrophage-specific oligonucleotide delivery, a molecular conjugate consisting of mannosylated polylysine that exploits endocytosis via the macrophage mannose receptor was used. Complexes were formed between the mannosylated polylysine and oligonucleotides and added to the cells in the presence of silica. Enzyme-linked immunoadsorbent assay showed that the complex consisting of the conjugate and antisense oligomer effectively inhibited TNF␣ production, whereas the oligomer alone had much less effect. Reverse transcriptase-polymerase chain reaction analysis revealed that the reduction in TNF␣ secretion was associated with specific ablation of targeted TNF␣ mRNA. The conjugate alone or conjugate complexed with inverted or sense sequence oligonucleotide had no effect. The promoting effect of the conjugate on antisense activity was shown to be due to enhanced cellular uptake of the oligomer via mannose receptor-mediated endocytosis. Cells lacking mannose receptors showed no susceptibility to the conjugate treatment. These results indicate that effective and selective inhibition of macrophage TNF␣ expression can be achieved using the antisense mannosylated polylysine system.

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“…Apart from acting as the primary nonspecific defense of the lung against inhaled PM, alveolar macrophages modulate the inflammatory response by secreting various mediators [10][11][12][13]. Oxidative stress may underlie the adverse health effects of many inhaled pollutants [14,15].…”

Section: Introductionmentioning

confidence: 99%

Effects of Atmospheric Particles and Several Model Particles of Particulate Matter Components on Human Monocyte-Derived Macrophage Oxidative Responses

Ohyama¹,

Akasaka²

2012

J Clin Toxicol

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Atmospheric particles are ingested by alveolar macrophages in the lung. The macrophages release reactive oxygen species on ingesting the particles. The aim of this study was to investigate the effect of particulate matter components on the release of reactive oxygen species from macrophages. We compared the effect of particulate matter with that of several model particles of particulate matter components, such as diesel exhaust particles, silica particles, two kinds of carbon black particles (a laser printer toner and an aggregation of laser printer toner), and 3-nitrobenzanthrone-coated carbon black particles, on the time course of induction of lucigenindependent chemiluminescence in human monocyte-derived macrophages. The particulate matter strongly induced chemiluminescence at lower concentrations. We observed similar chemiluminescence responses for particulate matter and 3-nitrobenzanthrone-coated carbon black particles. This result suggests that materials such as 3-nitrobenzanthrone are important contributors to the induction of reactive oxygen species by particulate matter. We also examined hydroxyl radical generation by the 2-deoxy-D-ribose method. Hydroxyl radical generation by particulate matter and diesel exhaust particles was greater than that by the other samples (the Mann-Whitney U test: p < 0.05). These results suggest that diesel exhaust and 3-nitrobenzanthrone-coated carbon black particles are insufficient as model particles of particulate matter components.

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Pulmonary Response to Silica or Titanium Dioxide: Inflammatory Cells, Alveolar Macrophage-derived Cytokines, and Histopathology

Cited by 230 publications

References 31 publications

Scavenger receptor class A type I/II (CD204) null mice fail to develop fibrosis following silica exposure

Scavenger receptor class A type I/II (CD204) null mice fail to develop fibrosis following silica exposure

Antisense Inhibition of Silica-induced Tumor Necrosis Factor in Alveolar Macrophages

Effects of Atmospheric Particles and Several Model Particles of Particulate Matter Components on Human Monocyte-Derived Macrophage Oxidative Responses

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