Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Nanoplastics dysregulate macrophage function by impairing glutathione metabolism

ABSTRACT: Micro- and nanoplastics (MNPs) are emerging environmental contaminants increasingly detected in human tissues. However, how MNP-related effector mechanisms that impact the immunological function of macrophages remain elusive. Here, we demonstrated that MNPs disrupt redox homeostasis and induce immune dysfunction in bone marrow-derived macrophages. MNP internalization in macrophages impairs mitochondrial function, inducing excessive and sustained production of reactive oxygen species along with suppressed glutathione metabolism, including the substantial down-regulation of key antioxidant enzymes, such as glutathione peroxidase (GPX) 1, GPX3, and GPX4. These processes cause oxidative imbalance, thereby triggering ferroptosis, compromising cellular integrity, and amplifying inflammatory signaling. Two-photon intravital and three-dimensional imaging in mice confirmed that orally administered MNPs accumulate in multiple organs. Such MNP accumulation exacerbates lung tumor progression, potentially through chronic inflammation and the immune dysregulation of macrophages. These findings reveal a novel mechanism by which MNPs alter innate immunity and promote an inflammatory microenvironment via redox-mediated ferroptosis.

ORGANISM(S): Mus musculus

PROVIDER: GSE299749 | GEO | 2025/06/18

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Nanoplastics dysregulate macrophage function by impairing glutathione metabolism

Project description:Nanoplastics dysregulate macrophage function by impairing glutathione metabolism

| PRJNA1276434 | ENA

Transcriptomic responses to transparent and blue PET micro-nanoplastics in Arabidopsis thaliana

Project description:To get further insights on the micro-nanoplastic (MNP) effects on plants, the aim of this study was to: 1) shed light on the transcriptome changes provoked by two different polyethylene terephthalate (PET) MNPs in plant roots; 2) determine their effects on key plant growth parameters in hydroponically-cultivated Arabidopsis thaliana. MNPs of transparent (Tr-PET) and blue (Bl-PET) material caused a significant reduction in root length, while only Bl-PET significantly reduced rosette area. Plant fresh and dry weight did not change, even though various OJIP-test parameters decreased in the presence of MNPs. RNA-seq data showed that Bl-PET and, especially, Tr-PET affected gene expression in comparison to controls. Tr-PET induced starch degradation and isoprenoids, while glycolysis, trehalose metabolism and fermentation were generally repressed. Tr-PET upregulated genes involved in signaling of xenobiotics, whereas Bl-PET scarcely affected root transcriptomic profile, activating few gene categories for abiotic stresses. Regarding hormones, genes involved in ABA response were repressed, while brassinosteroid-related genes were differentially regulated by Tr-PET. Both MNPs, but especially Tr-PET, upregulated major latex protein-related genes. These results allowed to gain insight into the effects of MNP contamination in plant metabolism, identifying targets for biotechnological strategies to enhance plant tolerance and phytoremediation of these xenobiotic agents.

2024-12-31 | E-MTAB-13532 | biostudies-arrayexpress

Xenium-based spatial transcriptomics of brains following chronic plastic exposure

Project description:Plastic pollution poses a universal yet understudied environmental risk to the immune system. Once ingested, nano- and microplastic particles (MNPs) can translocate from the gut into internal organs, likely via circulation. In humans, MNPs have been detected in macrophages within carotid artery plaques, suggesting that these highly phagocytic cells, may also serve as key targets for MNPs under homeostatic conditions. Kupffer cells (KCs), the liver-resident macrophages, play a crucial role in liver homeostasis by regulating metabolism, clearing opsonized target cells, and serving as the first line of defence against bacteria. Residing within the liver sinusoids, they continuously monitor the bloodstream, efficiently capturing and eliminating pathogens and circulating particles to maintain immune and metabolic balance5. It remains unknown whether KCs efficiently capture and store MNPs and how this might affect liver function. Here, we utilize a mouse model of chronic plastic exposure to assess how ingested MNP influence KC core functions, and thereby also liver function. We show that KCs are the primary hepatic target of MNPs and that 12 weeks of exposure alters their transcriptome and impairs phagocytic capacity, leading to dysregulated liver metabolism. Microplastics, but not nanoplastics, exposure reduces KC-mediated clearance of circulating cells and bacteria and exacerbates diet-induced obesity. These findings suggest that chronic MNP exposure disrupts tissue-specific macrophage functions in a size-dependent manner, with distinct long-term consequences for liver function and overall health.

2025-03-12 | GSE291378 | GEO

Single-cell analysis reveals Mycobacterium tuberculosis ESX-1–mediated accumulation of permissive macrophages in infected mouse lungs

Project description:Mycobacterium tuberculosis (MTB) infects and replicates in lung mononuclear phagocytes (MNPs) with astounding ability to evade elimination. A virulence determinant that contributes to MTB’s ability to survive within MNPs is ESX-1, a type VII secretion system. However, how MTB virulence factors influence mononuclear cell recruitment and/or differentiation remains unknown. Here, using single-cell RNA sequencing, we studied the role of ESX-1 in MNP heterogenicity and response in mice and murine bone marrow-derived macrophages. We found that ESX-1 is required for MTB to recruit diverse MNP subsets with high MTB burden. Further, MTB induces an anti-inflammatory signature that may lead to more permissive MNPs. Spatial transcriptomics revealed an upregulation of anti-inflammatory signals in MTB lesions, where monocyte-derived macrophages concentrate near MTB-infected cells. Together, our findings suggest that MTB ESX-1 mediates the recruitment and differentiation of anti-inflammatory MNPs, which MTB can infect and manipulate for survival.

2024-04-20 | GSE263880 | GEO

Single-cell analysis reveals Mycobacterium tuberculosis ESX-1–mediated accumulation of permissive macrophages in infected mouse lungs

2024-04-20 | GSE263891 | GEO

Single-cell analysis reveals Mycobacterium tuberculosis ESX-1–mediated accumulation of permissive macrophages in infected mouse lungs

2024-04-20 | GSE263882 | GEO

Cross-tissue single cell landscape of human monocytes and macrophages in health and disease

Project description:Mononuclear phagocytes (MNP) encompass dendritic cells, monocytes and macrophages (MoMac), which exhibit antimicrobial, homeostatic and immunoregulatory functions. We integrated 178,651 MNP from 13 tissues across 41 datasets to generate a MNP single-cell RNA compendium (MNP-VERSE), a publicly available tool to map MNPs and defined conserved gene signatures of MNP populations. Next, we generated a MoMac-focused compendium that revealed an array of specialised cell subsets widely distributed across multiple tissues. Specific pathological forms were expanded in cancer and inflammation. All neoplastic tissues contained conserved tumour-associated macrophage populations. Particularly, we focused on IL4I1+CD274(PD-L1)+IDO1+ macrophages, which accumulated in the tumour periphery in a T cell-dependent manner via IFNg and CD40/CD40L-induced maturation from interferon-primed monocytes. IL4I1_Macs exhibited immune-suppressive characteristics through tryptophan degradation and promoted entry of regulatory T cell into tumours. This integrated analysis provides a robust online-available platform for uniform annotation and dissection of specific macrophage functions in healthy and pathological states.

2021-06-16 | GSE178209 | GEO

Nanoplastics Enhance Transmembrane Transport of Carcinogens and Induce Cellular Stress Responses as Revealed by mRNA Sequencing Analysis

Project description:Nanoplastics were generated from common consumer plastics (PET, HDPE, PS, PVC) and exposed to simulated marine weathering for up to 10 weeks. Fourier-Transform Infrared (FT-IR) spectroscopy and ζ-potentials measurements revealed continuous changes in the composition of the nanoplastics consistent with oxidation. Although the chemical composition and oxidation of the nanoplastics influenced their ability to sorb Polycyclic Aromatic Hydrocarbons (PAHs), for all investigated conditions, sorption of PAH to nanoplastics achieved effective PAH concentrations that were orders of magnitude higher than the solubility limit in water. In an intestinal membrane model, PAH-loaded nanoplastics enhanced the overall PAH transport into and across the membrane, with HDPE achieving the highest intracellular PAH concentration. RNA sequencing of cell membranes exposed to nanoplastics revealed significant transcriptional changes, including upregulation of oxidative stress and detoxification pathways (NQO1, CYP1A1, CYP1B), especially in response to PAH-loaded nanoplastics, while genes associated with basic cell functions, such as cellular migration (NCKAP5, MACROD2) and division (KIF20A) were downregulated. These findings suggest that nanoplastics can increase bioaccessibility and bioavailability of hydrophobic carcinogens and enhance cellular stress, raising concerns about the potential environmental and health impacts associated with nanoplastics as carriers of hydrophobic environmental toxins.

2025-06-20 | GSE281152 | GEO

Nanoplastics-16s

Project description:Nanoplastics-16s Raw sequence reads

| PRJNA948176 | ENA

Gut-Lung Microbiota Dynamics in Mice Exposed to Nanoplastics

Project description:The objective was to evaluate the impact of nanoplastics on various niches of the microbiome in a mouse model

2024-10-21 | GSE265766 | GEO