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Lung macrophages "digest" carbon nanotubes using a superoxide/peroxynitrite oxidative pathway.

ABSTRACT: In contrast to short-lived neutrophils, macrophages display persistent presence in the lung of animals after pulmonary exposure to carbon nanotubes. While effective in the clearance of bacterial pathogens and injured host cells, the ability of macrophages to "digest" carbonaceous nanoparticles has not been documented. Here, we used chemical, biochemical, and cell and animal models and demonstrated oxidative biodegradation of oxidatively functionalized single-walled carbon nanotubes via superoxide/NO* ? peroxynitrite-driven oxidative pathways of activated macrophages facilitating clearance of nanoparticles from the lung.

SUBMITTER: Kagan VE

PROVIDER: S-EPMC4072413 | biostudies-literature | 2014 Jun

REPOSITORIES: biostudies-literature

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Lung macrophages "digest" carbon nanotubes using a superoxide/peroxynitrite oxidative pathway.

Kagan Valerian E VE Kapralov Alexandr A AA St Croix Claudette M CM Watkins Simon C SC Kisin Elena R ER Kotchey Gregg P GP Balasubramanian Krishnakumar K Vlasova Irina I II Yu Jaesok J Kim Kang K Seo Wanji W Mallampalli Rama K RK Star Alexander A Shvedova Anna A AA

ACS nano 20140604 6

In contrast to short-lived neutrophils, macrophages display persistent presence in the lung of animals after pulmonary exposure to carbon nanotubes. While effective in the clearance of bacterial pathogens and injured host cells, the ability of macrophages to "digest" carbonaceous nanoparticles has not been documented. Here, we used chemical, biochemical, and cell and animal models and demonstrated oxidative biodegradation of oxidatively functionalized single-walled carbon nanotubes via superoxid ...[more]

PMID: 24871084

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Carbon nanotubes, but not graphene oxide, trigger chemokine production in primary human macrophages via MyD88 dependent NF-kB Pathway

Project description:The growing medical application of engineered nanomaterials (ENMs) necessitates better understanding of their molecular toxicity mechanisms governing immune effects. In the present study, a comprehensive mechanistic in vitro assessment of two carbon-based ENMs, single-walled carbon nanotubes (SWCNTs) and graphene oxide (GO), was performed using primary human monocyte-derived macrophages (HMDM) as a model. HMDM were exposed to SWCNTs and GO at concentrations 10–100 µg/ml for 24 h. Toxicity, reactive oxygen species (ROS) production and uptake of ENM by cells was measured. The changes in gene expression profile of HMDM in response to SWCNTs and GO were studied and the key stress response pathways identified. The transcriptomics and pathway enrichment analysis findings were verified by multiplex immunoassay and functional assays.

2017-09-30 | GSE83516 | GEO

Monocytic ontogeny of regenerated macrophages characterizes the mesotheliomagenic responses to carbon nanotubes

Project description:Macrophages not only derive from circulating blood monocytes, but also originate from embryonic progenitors that can proliferate. This dichotomic origin has an impact on macrophage functions in steady state and pathological conditions. Long needle-like carbon nanotubes (CNT) damage serous membranes and induce mesothelioma like asbestos fibers. Macrophages predominantly infiltrate CNT-induced injured tissue and contribute to cancer development. Here, we revealed the exact ontogeny of macrophage populations after CNT exposure by comparing the response to needle-like mesotheliomagenic CNT-7 with tangled-like non-mesotheliomagenic CNT-T. In a rat peritoneal cavity model, both CNT induced a rapid and complete depletion of MHCIIlow resident macrophages generating an empty niche available for macrophage repopulation. Macrophage disappearance after mesotheliomagenic CNT-7 was followed by a substantial inflammatory reaction, and macrophage replenishment completed after 7 days. Fifteen days after non-mesotheliomagenic CNT-T, macrophage repopulation was incomplete and accompanied by a limited inflammatory reaction. Cell depletion experiments, flow cytometry and RNA-seq analysis demonstrated that, after CNT-7, resident macrophages were mainly replaced by an influx of monocytes, which differentiated locally into MHCIIhigh inflammatory macrophages. In contrast, the low inflammatory response induced by CNT-T was linked to the activation of self-renewing MHCIIlow macrophages. In conclusion, the mesotheliomagenic response to CNT specifically relies on macrophage niche recolonization by monocytic progenitors. The homeostasis returns after exposure to non mesotheliomagenic CNT-T involves, in contrast, a macrophage maintenance by proliferation. Macrophage depletion and repopulation are thus decisive events characterizing the carcinogenic activity of fibrous particles.

2020-09-05 | GSE157487 | GEO

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