ArticleParticle and fibre toxicology2025
Combustion-derived carbon nanoparticles cause delayed apoptosis in neutrophil-like HL-60 cells in vitro and in primed human neutrophilic granulocytes ex vivo.
Article in Particle and fibre toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- SPTLC2-driven sphingolipid reprogramming of neutrophils impairs anti-tumour immunity and drives liver cancer progression.Oncogene · 2026Article
- Article
- Compatible Solutes Prevent Lung Inflammation and Reduction in CFTR Induced by Combustion-Derived Nanoparticles in Human and Rodent Experimental Systems.International journal of molecular sciences · 2025Article
- Charting new frontiers in nanoparticle immunotoxicity: A perspective on current, emerging, and future approaches.Biochemical and biophysical research communications · 2025Review
- Article
- Differentiation of HL-60 cells into primed neutrophils for the evaluation of antiapoptotic effects of poorly soluble nanoparticles.PloS one · 2025Article
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Funding
Abstract
backgroundInhalation of combustion-derived nanoparticles may contribute to the development or exacerbation of inflammatory lung diseases by direct interaction with neutrophilic granulocytes. Earlier studies have shown that exposure of human neutrophils to carbon nanoparticles ex vivo causes a prolongation of cellular life by the reduction of apoptosis rates. Accordingly, reduced neutrophil apoptosis rates were observed in neutrophils from bronchoalveolar lavages from carbon nanoparticle-exposed animals. The current study describes molecular and cellular modes of action responsible for this proinflammatory effect.
resultsExperiments with human blood neutrophils or neutrophil-like differentiated HL-60 cells exposed to carbon nanoparticles revealed dose dependent reduction of apoptosis rates. In both experimental systems, intracellular reactive oxygen species proved to be causally linked to this endpoint. Among the human samples, only primed cells from donors with slightly elevated proinflammatory plasma factors responded by delayed apoptosis. These neutrophils are characterized by an immunophenotype (CD16
conclusionsThe antiapoptotic reactions observed in two independent experimental systems, differentiated neutrophil-like HL-60 cells and primed neutrophils, may be considered as additional proinflammatory effect of inhaled combustion-derived nanoparticles. Particularly in chronic diseases, which are characterized by neutrophilic lung inflammation, this effect can be expected to contribute to the deterioration of the health status. The data describe a mode of action in which intracellular reactive oxygen species cause membrane rearrangements that are responsible for neutrophil activation and delayed apoptosis.
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