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Carbon-based functional nanomaterials have attracted immense scientific interest from many disciplines and, due to their extraordinary properties, have offered tremendous potential in a diverse range of applications. Among the different carbon nanomaterials, graphene is one of the newest and is considered the most important. Graphene, a monolayer material composed of sp-hybridized carbon atoms hexagonally arranged in a two-dimensional structure, can be easily functionalized by chemical modification. Functionalized graphene and its derivatives have been used in diverse nano-biotechnological applications, such as in environmental engineering, biomedicine, and biotechnology. However, the prospective use of graphene-related materials in a biological context requires a detailed comprehension of these materials, which is essential for expanding their biomedical applications in the future. In recent years, the number of biological studies involving graphene-related nanomaterials has rapidly increased. These studies have documented the effects of the biological interactions between graphene-related materials and different organizational levels of living systems, ranging from biomolecules to animals. In the present review, we will summarize the recent progress in understanding mainly the interactions between graphene and cells. The impact of graphene on intracellular components, and especially the uptake and transport of graphene by cells, will be discussed in detail.

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Epidemiological studies have associated high levels of airborne particulate matter (PM) with increased respiratory diseases. In order to investigate the mechanisms of air pollution-induced lung toxicity in humans, human bronchial epithelial cells (16HBE) were exposed to various concentrations of particles smaller than 2.5 μm (PM2.5) collected from Beijing, China. After observing that PM2.5 decreased cell viability in a dose-dependent manner, we first used Illumina RNA-seq to identify genes and pathways that may contribute to PM2.5-induced toxicity to 16HBE cells. A total of 539 genes, 283 up-regulated and 256 down-regulated, were identified to be significantly differentially expressed after exposure to 25 μg/cm2 PM2.5. PM2.5 induced a large number of genes involved in responses to xenobtiotic stimuli, metabolic response, and inflammatory and immune response pathways such as MAPK signaling and cytokine-cytokine receptor interaction, which might contribute to PM2.5-related pulmonary diseases. We then confirmed our RNA-seq results by qPCR and by analysis of IL-6, CYP1A1, and IL-8 protein expression. Finally, ELISA assay demonstrated a significant association between exposure to PM2.5 and secretion of IL-6. This research provides a new insight into the mechanisms underlying PM2.5-induced respiratory diseases in Beijing.