Combustion-derived carbon nanoparticles cause delayed apoptosis in neutrophil-like HL-60 cells in vitro and in primed human neutrophilic granulocytes ex vivo

The 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.