Mayes Alswady-Hoff

National Institute of Occupational Health

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Shanbeh Zienolddiny

National Institute of Occupational Health

ØS

Øivind Skare

National Institute of Occupational Health

Johanna Samulin Erdem

National Institute of Occupational Health

Animesh Sharma

Central Norway Regional Health Authority

Yke Jildouw Arnoldussen

National Institute of Occupational Health

Torunn Ervik

National Institute of Occupational Health

Erik Ropstad

Norwegian University of Life Sciences

Vidar Skaug

Vera Institute of Justice

Kristine Haugen Anmarkrud

National Institute of Occupational Health

Geir Slupphaug

Norwegian University of Science and Technology

Cooperative Institutions

National Institute of Occupational Health

University of Oslo

Norwegian University of Science and Technology

Oslo University Hospital

Central Norway Regional Health Authority

St Olav's University Hospital

Norwegian University of Life Sciences

657 Oslo

Norwegian Veterinary Institute

The University of Texas MD Anderson Cancer Center

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Multiwalled Carbon Nanotubes Induce Fibrosis and Telomere Length Alterations

International Journal of Molecular Sciences (2022)

Mayes Alswady-Hoff Johanna Samulin Erdem Mona Aleksandersen Kristine Haugen Anmarkrud Øivind Skare

Telomere shortening can result in cellular senescence and in increased level of genome instability, which are key events in numerous of cancer types. Despite this, few studies have focused on the effect of nanomaterial exposure on telomere length as a possible mechanism involved in nanomaterial-induced carcinogenesis. In this study, effects of exposure to multiwalled carbon nanotubes (MWCNT) on telomere length were investigated in mice exposed by intrapleural injection, as well as in human lung epithelial and mesothelial cell lines. In addition, cell cycle, apoptosis, and regulation of genes involved in DNA damage repair were assessed. Exposure to MWCNT led to severe fibrosis, infiltration of inflammatory cells in pleura, and mesothelial cell hyperplasia. These histological alterations were accompanied by deregulation of genes involved in fibrosis and immune cell recruitment, as well as a significant shortening of telomeres in the pleura and the lung. Assessment of key carcinogenic mechanisms in vitro confirmed that long-term exposure to the long MWCNT led to a prominent telomere shortening in epithelial cells, which coincided with G1-phase arrest and enhanced apoptosis. Altogether, our data show that telomere shortening resulting in cell cycle arrest and apoptosis may be an important mechanism in long MWCNT-induced inflammation and fibrosis.

Senescence

10.3390/ijms23116005

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Citations (6)

P02-06 New Approach Methodologies for hepatotoxic hazard assessment: development of an in vitro human liver fibrosis model

Toxicology Letters (2024)

G. Lopez Soop L. Wik Mayes Alswady-Hoff Shanbeh Zienolddiny Sarah Mollerup

10.1016/j.toxlet.2024.07.276

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Long-Term Exposure to Nanosized TiO2 Triggers Stress Responses and Cell Death Pathways in Pulmonary Epithelial Cells

International Journal of Molecular Sciences (2021)

Mayes Alswady-Hoff Johanna Samulin Erdem Santosh Phuyal Oskar Knittelfelder Animesh Sharma

There is little in vitro data available on long-term effects of TiO2 exposure. Such data are important for improving the understanding of underlying mechanisms of adverse health effects of TiO2. Here, we exposed pulmonary epithelial cells to two doses (0.96 and 1.92 µg/cm2) of TiO2 for 13 weeks and effects on cell cycle and cell death mechanisms, i.e., apoptosis and autophagy were determined after 4, 8 and 13 weeks of exposure. Changes in telomere length, cellular protein levels and lipid classes were also analyzed at 13 weeks of exposure. We observed that the TiO2 exposure increased the fraction of cells in G1-phase and reduced the fraction of cells in G2-phase, which was accompanied by an increase in the fraction of late apoptotic/necrotic cells. This corresponded with an induced expression of key apoptotic proteins i.e., BAD and BAX, and an accumulation of several lipid classes involved in cellular stress and apoptosis. These findings were further supported by quantitative proteome profiling data showing an increase in proteins involved in cell stress and genomic maintenance pathways following TiO2 exposure. Altogether, we suggest that cell stress response and cell death pathways may be important molecular events in long-term health effects of TiO2.

Proteome

10.3390/ijms22105349

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Cellulose nanocrystals modulate alveolar macrophage phenotype and phagocytic function

Biomaterials (2019)

Johanna Samulin Erdem Mayes Alswady-Hoff Torunn Ervik Øivind Skare Dag G. Ellingsen

Nanocellulose is a promising bio-nanomaterial with attractive properties suitable for multiple industrial applications. The increased use of nanocellulose may lead to occupational exposure and negative health outcomes. However, knowledge on its health effects is limited, and while nanocellulose exposure may induce acute inflammatory responses in the lung, the underlying mechanisms are unknown. Alveolar macrophages are key cells in alveolar particle clearance. Their activation and function may be affected by various particles. Here, we investigated the uptake of pristine cellulose nanocrystals (CNC), and their effects on alveolar macrophage polarization and biological function. CNC uptake enhanced the secretion of several cytokines but did not on its own induce a complete macrophage polarization. In presence of macrophage activators, such as LPS/IFNG and IL4/IL13, CNC exposure enhanced the expression of M1 phenotype markers and the secretion of pro-inflammatory cytokines and chemokines, while decreasing M2 markers. CNC exposure also affected the function of activated alveolar macrophages resulting in a prominent cytokine burst and altered phagocytic activity. In conclusion, CNC exposure may result in dysregulation of macrophage activation and function that are critical in inflammatory responses in the lung.

Nanocellulose

Alveolar macrophage

Macrophage polarization

Proinflammatory cytokine

10.1016/j.biomaterials.2019.02.025

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Citations (34)