Pulmonary Macrophages

Laskin, Debra L.; Malaviya, Rama; Laskin, Jeffrey D.

doi:10.1016/b978-0-12-404577-4.00032-1

Cited by 9 publications

(6 citation statements)

References 210 publications

(358 reference statements)

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“…The present studies show that mannose receptor is constitutively expressed on resident alveolar macrophages, which is consistent with previous reports (Laskin et al, 2015). Following WTC dust exposure, macrophage expression of mannose receptor was down regulated at 3 d and 7 d, suggesting an early impairment of phagocytosis.…”

Section: Discussionsupporting

confidence: 94%

World Trade Center (WTC) dust exposure in mice is associated with inflammation, oxidative stress and epigenetic changes in the lung

Sunil

Vayas

Fang

et al. 2017

Experimental and Molecular Pathology

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Exposure to World Trade Center (WTC) dust has been linked to respiratory disease in humans. In the present studies we developed a rodent model of WTC dust exposure to analyze lung oxidative stress and inflammation, with the goal of elucidating potential epigenetic mechanisms underlying these responses. Exposure of mice to WTC dust (20 μg, i.t.) was associated with upregulation of heme oxygenase-1 and cyclooxygenase-2 within 3 days, a response which persisted for at least 21 days. Whereas matrix metalloproteinase was upregulated 7 days post-WTC dust exposure, IL-6RA1 was increased at 21 days; conversely, expression of mannose receptor, a scavenger receptor important in particle clearance, decreased. After WTC dust exposure, increases in methylation of histone H3 lysine K4 at 3 days, lysine K27 at 7 days and lysine K36, were observed in the lung, along with hypermethylation of Line-1 element at 21 days. Alterations in pulmonary mechanics were also observed following WTC dust exposure. Thus, 3 days post-exposure, lung resistance and tissue damping were decreased. In contrast at 21 days, lung resistance, central airway resistance, tissue damping and tissue elastance were increased. These data demonstrate that WTC dust-induced inflammation and oxidative stress are associated with epigenetic modifications in the lung and altered pulmonary mechanics. These changes may contribute to the development of WTC dust pathologies.

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Section: Discussionsupporting

confidence: 94%

World Trade Center (WTC) dust exposure in mice is associated with inflammation, oxidative stress and epigenetic changes in the lung

Sunil

Vayas

Fang

et al. 2017

Experimental and Molecular Pathology

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“…Alveolar macrophages (AMs) are the housekeepers of the lung. Aside from participating in local homeostasis, such as the recycling of surfactant components and efferocytosis, they are equipped and armed to deal with particles that get deep into the alveolar region from inorganic particulate matter to saprophytic and pathogenic microflora (Laskin, Malaviya, and Laskin, 2015). Importantly, alveolar macrophages contribute to the overall tolerant immunological milieu, possessing the so-called M2-like phenotype in the resting state (Alber, Howie, Wallace, and Hirani, 2012).…”

Section: Discussionmentioning

confidence: 99%

Comparative cytotoxicity of respirable surface-treated/untreated calcium carbonate rock dust particles in vitro

Khaliullin

Kisin

Yanamala

et al. 2019

Toxicology and Applied Pharmacology

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Calcium carbonate rock dust (RD) is used in mining to reduce the explosivity of aerosolized coal. During the dusting procedures, potential for human exposure occurs, raising health concerns. To improve RD aerosolization, several types of anti-caking surface treatments exist. The aim of the study was to evaluate cytotoxicity of four respirable RD samples: untreated/treated limestone (UL/TL), untreated/treated marble (UM/TM), and crystalline silica (SiO2) as a positive control in A549 and THP-1 transformed human cell lines. Respirable fractions were generated and collected using FSP10 high flow-rate cyclone samplers. THP-1 cells were differentiated with phorbol-12-myristate-13-acetate (20 ng/ml, 48 h). Cells were exposed to seven different concentrations of RD and SiO2 (0–0.2 mg/ml). RD caused a slight decrease in viability at 24 or 72 h post-exposure and were able to induce inflammatory cytokine production in A549 cells, however, with considerably less potency than SiO2. In THP-1 cells at 24 h, there was significant dose-dependent lactate dehydrogenase, inflammatory cytokine and chemokine release. Caspase-1 activity was increased in SiO2- and, on a lesser scale, in TM- exposed cells. To test if the increased toxicity of TM was uptake-related, THP-1 cells were pretreated with Cytochalasin D (CytD) or Bafilomycin A (BafA), followed by exposure to RD or SiO2 for 6 h. CytD blocked the uptake and significantly decreased cytotoxicity of all particles, while BafA prevented caspase-1 activation but not cytotoxic effects of TM. Only TM was able to induce an inflammatory response in THP-1 cells, however it was much less pronounced compared to silica.

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“…To address this, we expose a co-culture of LA-4 epithelial cells and MH-S alveolar macrophages in the same way as we did with the epithelial monoculture. With a co-culture of MH-S alveolar macrophages on top of nearly confluent LA-4 epithelial cells we aimed to mimic the cell populations of the alveolar surface, where alveolar macrophages represent approximately 3-5% of all the alveolar cells 37 . Upon exposure of the co-culture to TiO2 nanotubes, part of the material gets internalized by the phagocytes, which cannot entirely prevent nanomaterial from reaching epithelial cells (SI section S0h ), and is in line with previous studies 38 .…”

Section: The Role Of Actinmentioning

confidence: 99%

From the Roundabout of Molecular Events to Nanomaterial-Induced Chronic Inflammation Prediction

Majaron

Kokot

Sebastijanović

et al. 2020

Preprint

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Many chronic diseases manifest in prolonged inflammation and often ignored dysregulated lipid metabolism. When associated with inhalation of nanomaterials, limited information is available on the relevant molecular events and their causal connections. This prevents reliable prediction of outcomes by efficient testing strategies. To unravel how acute nanomaterial exposure leads to chronic conditions, we employed advanced microscopy and omics in vitro and in vivo together with in silico modelling.For selected metal-oxide nanomaterials, we show that lung epithelial cells survive the exposure by excreting internalized nanomaterials and passivating them on the surface, employing elevated lipid synthesis. Macrophages, on the contrary, lose their integrity whilst degrading the passivized bio-nano agglomerates, releasing the nanomaterials, which are taken up again by the epithelial cells. Constant proinflammatory signalling recruits new phagocytes that feed the vicious cycle of events, resulting in a long-lasting response to a single exposure. The proposed mechanism explains the nanomaterialassociated in vivo chronic outcomes and allows its prediction based on in vitro measurements. Similar mechanisms may trigger other chronic diseases affecting millions of lives worldwide.

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Pulmonary Macrophages

Cited by 9 publications

References 210 publications

World Trade Center (WTC) dust exposure in mice is associated with inflammation, oxidative stress and epigenetic changes in the lung

World Trade Center (WTC) dust exposure in mice is associated with inflammation, oxidative stress and epigenetic changes in the lung

Comparative cytotoxicity of respirable surface-treated/untreated calcium carbonate rock dust particles in vitro

From the Roundabout of Molecular Events to Nanomaterial-Induced Chronic Inflammation Prediction

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