Graphene Particles Interfere with Pro‐Inflammatory Polarization of Human Macrophages: Functional and Electrophysiological Evidence

The interaction of two types of fragmented graphene particles (30–160 nm) with human macrophages is studied. Since macrophages have significant phagocytic activity, the incorporation of graphene particles into cells has an effect on the response to functional polarization stimuli, favoring an anti‐inflammatory profile. Incubation of macrophages with graphene foam particles, prepared by chemical vapor deposition, and commercially available graphene nanoplatelet particles does not affect cell viability when added at concentrations up to 100 µg mL−1; macrophages exhibit differential quantitative responses to each type of graphene particles. Although both materials elicit similar increases in the release of reactive oxygen species, the impact on the transcriptional regulation associated with the polarization profile is different; graphene nanoplatelets significantly modify this transcriptomic profile. Moreover, these graphene particles differentially affect the motility and phagocytosis of macrophages. After the incorporation of both graphene types into the macrophages, they exhibit specific responses in terms of the mitochondrial oxygen consumption and electrophysiological potassium currents at the cell plasma membrane. These data support the view that the physical structure of the graphene particles has an impact on human macrophage responses, paving the way for the development of new mechanisms to modulate the activity of the immune system. The interaction of human macrophages with graphene particles improves the production of reactive oxygen species without altering their viability. Graphene particles are incorporated by macrophages altering the transcriptional control of genes involved in the pro‐inflammatory and pro‐resolution responses. Furthermore, the phagocytosed graphene particles modify the mitochondrial oxygen consumption, which offers novel possibilities to modulate the immune response of human macrophages.