Response of Alveolar Macrophages to Inhaled Particulates

Dörger, Martina; Krombach, Fritz

doi:10.1159/000048887

Cited by 14 publications

(7 citation statements)

References 55 publications

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“…After phagocytosis of inhaled organic dust, mineral fibers, or fungal spores, activated alveolar macrophages secrete a variety of cytokines that are involved in the development and maintenance of inflammatory response (Vanhée et al, 1995;Driscoll, 2000;Dörger and Krombach, 2002;Mansour and Levitz, 2002;Yucesoy et al, 2002). In the present study, all the tested wood dust species induced a dose-dependent increase in the TNF-␣ production at protein level.…”

Section: Discussionsupporting

confidence: 47%

“…All these inflammatory diseases are characterized by the infiltration of inflammatory cells (T cells, mast cells, basophils, eosinophils, neutrophils, and/or macrophages) to the site of inflammation (Owen, 2001;McSharry et al, 2002;Sebastiani et al, 2002;Stahl et al, 2002;Hamid et al, 2003). Several previous studies have shown that activated alveolar macrophages secrete after phagocytosis of inhaled organic dust, mineral fibers, or fungal spores a variety of cytokines and chemokines that are involved in the development and maintenance of inflammatory response (Vanhée et al, 1995;Driscoll, 2000;Dörger and Krombach, 2002;Mansour and Levitz, 2002;Yucesoy et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

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Comparison of hardwood and softwood dust-induced expression of cytokines and chemokines in mouse macrophage RAW 264.7 cells

et al. 2006

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Section: Discussionsupporting

confidence: 47%

Section: Introductionmentioning

confidence: 99%

Comparison of hardwood and softwood dust-induced expression of cytokines and chemokines in mouse macrophage RAW 264.7 cells

et al. 2006

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“…Elemental carbon-based nanoparticles with a diameter of less than 100 nm are a major part of diesel exhaust and ambient pollution. After deposition in the lungs, larger particles are phagocytized by alveolar and airway macrophages [6, 7], but the fine and ultrafine carbon particles remain in the lungs for a longer period of time [8]. Ultrafine particles are phagocytized to a minor extend but they can still enter macrophages and epithelial cells and even penetrate into the circulation.…”

Section: Introductionmentioning

confidence: 99%

Carbon Black Particle Exhibits Size Dependent Toxicity in Human Monocytes

Sahu

Kannan

Vijayaraghavan

2014

International Journal of Inflammation

118

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Increased levels of particulate air pollution are associated with increased respiratory and cardiovascular mortality and morbidity. Some epidemiologic and toxicological researches suggest ultrafine particles (<100 nm) to be more harmful per unit mass than larger particles. In the present study, the effect of particle size (nano and micro) of carbon black (CB) particle on viability, phagocytosis, cytokine induction, and DNA damage in human monocytes, THP-1 cells, was analysed. The cells were incubated with nanosize (~50 nm) and micron (~500 nm) size of CB particles in a concentration range of 50–800 µg/mL. The parameters like MTT assay, phagocytosis assay, ELISA, gene expression, and DNA analysis were studied. Exposure to nano- and micron-sized CB particles showed size- and concentration dependent decrease in cell viability and significant increase in proinflammatory cytokines IL-1β, TNF-α and IL-6 as well as chemokine IL-8 release. Gene expression study showed upregulation of monocyte chemoattractant protein-1 gene while cyclooxygenase-2 gene remained unaffected. Nano CB particles altered the phagocytic capacity of monocytes although micron CB had no significant effect. CB particles did not show any significant effect on DNA of monocytes. The investigations indicate that CB particles in nanosize exhibit higher propensity of inducing cytotoxicity, inflammation, and altered phagocytosis in human monocytes than their micron size.

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“…Inhalation of toxin-containing SC spores or free toxin-contaminated dust particulates is the major route of human exposure in indoor environments [5]. The inhaled toxic particulates containing trichothecene mycotoxins are subjected to phagocytosis and clearance by the host alveolar macrophages (AMs), which act as a critical first line of innate defense in the host lung against inhaled particulates [6]. Our studies have shown that the toxins associated with SC spores cause cell death and cytotoxicity in the exposed alveolar macrophages [7].…”

Section: Introductionmentioning

confidence: 99%

Global gene expression changes underlying Stachybotrys chartarum toxin-induced apoptosis in murine alveolar macrophages: Evidence of multiple signal transduction pathways

Wang

Yadav

2006

Apoptosis

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The overall mechanism(s) underlying macrophage apoptosis caused by the toxins of the indoor mold Stachybotrys chartarum (SC) are not yet understood. In this direction, we report a microarray-based global gene expression profiling on the murine alveolar macrophage cell line (MH-S) treated with SC toxins for short (2 h) and long (24 h) periods, coinciding with the pre-apoptotic (<3 h) and progressed apoptotic stages of the treated cells, respectively. Microarray results on differential expression were validated by real-time RT-PCR analysis using representative gene targets. The toxin-regulated genes corresponded to multiple cellular processes, including cell growth, proliferation and death, inflammatory/immune response, genotoxic stress and oxidative stress, and to the underlying multiple signal transduction pathways involving MAPK-, NF-kB-, TNF-, and p53-mediated signaling. Transcription factor NF-kB showed dynamic temporal changes, characterized by an initial activation and a subsequent inhibition. Up-regulation of a battery of DNA damage-responsive and DNA repair genes in the early stage of the treatment suggested a possible role of genotoxic stress in the initiation of apoptosis. Simultaneous expression changes in both pro-survival genes and pro-apoptotic genes indicated the role of a critical balance between the two processes in SC toxin-induced apoptosis. Taken together, the results imply that multiple signaling pathways underlie the SC toxin-induced apoptosis in alveolar macrophages.

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Response of Alveolar Macrophages to Inhaled Particulates

Cited by 14 publications

References 55 publications

Comparison of hardwood and softwood dust-induced expression of cytokines and chemokines in mouse macrophage RAW 264.7 cells

Comparison of hardwood and softwood dust-induced expression of cytokines and chemokines in mouse macrophage RAW 264.7 cells

Carbon Black Particle Exhibits Size Dependent Toxicity in Human Monocytes

Global gene expression changes underlying Stachybotrys chartarum toxin-induced apoptosis in murine alveolar macrophages: Evidence of multiple signal transduction pathways

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