Carbon nanomaterials (CNM) are targets of great interest because they have multiple applications in industry but also because of the fear of possible harmful heath effects of certain types of CNM. The high aspect ratio of carbon nanotubes (CNT), a feature they share with asbestos, is likely the key factor for reported toxicity of certain CNT. However, the mechanism to explain this toxicity is unclear. Here we investigated whether different CNM induce a pro-inflammatory response in human primary macrophages. Carbon black, short CNT, long, tangled CNT, long, needle-like CNT, and crocidolite asbestos were used to compare the effect of size and shape on the potency of the materials to induce secretion of interleukin (IL) 1-family cytokines. Our results demonstrated that long, needle-like CNT and asbestos activated secretion of IL-1β from LPS-primed macrophages but only long, needle-like CNT induced IL-1α secretion. SiRNA experiments demonstrated that the NLRP3 inflammasome was essential for long, needle-like CNT and asbestos-induced IL-1β secretion. Moreover, it was noted that CNT-induced NLRP3 inflammasome activation depended on reactive oxygen species (ROS) production, cathepsin B activity, P2X(7) receptor, and Src and Syk tyrosine kinases. These results provide new information about the mechanisms by which long, needle-like materials may cause their harmful health effects. Furthermore, the techniques used here may be of use in future risk assessments of nanomaterials.

Adsorption of proteins onto an engineered nanoparticle surface happens immediately after particles come in contact with a biological fluid. However, at the moment very little is known about the mechanisms of interactions between biomolecules and nanomaterials. In this study, eleven thoroughly characterized materials were first investigated in vitro for their ability to enter human lung epithelial cells and human monocyte-derived macrophages. All tested materials were taken up by primary macrophages and epithelial cells. Some of the engineered nanomaterials (ENM) were found in the cytoplasm. Large quantitative and qualitative variation in the binding efficiencies to cellular proteins was observed between different tested nanoparticles. Pulmonary surfactant components significantly reduced the overall protein adsorption on the surface of ENMs. Fibrinogen chains were attached to all materials after exposure to plasma proteins. Common ENM-bound cytoplasmic protein identifications were peroxiredoxin 1, annexin A2, and several ribosomal and cytoskeletal proteins. The underlying mechanism of the ENM-plasma protein interaction may diverge from that of cell lysate proteins, as the binding efficiency to cell lysate proteins appears to depend on the characteristics of the ENM surface, whereas the adsorbed plasma proteins are involved in particle phagocytosis and seem to cover ENMs independently of the their surface properties. Identification of the composition of the nanomaterial-protein complex is crucial for understanding of the uptake mechanisms, biodistribution, and clearance of ENMs, knowledge which is required for safety evaluation and biomedical applications of these materials.

Only a few archaeal viruses have been subjected to detailed structural analyses. Major obstacles have been the extreme conditions such as high salinity or temperature needed for the propagation of these viruses. In addition, unusual morphotypes of many archaeal viruses have made it difficult to obtain further information on virion architectures. We used controlled virion dissociation to reveal the structural organization of Halorubrum pleomorphic virus 1 (HRPV-1) infecting an extremely halophilic archaeal host. The singlestranded DNA genome is enclosed in a pleomorphic membrane vesicle without detected nucleoproteins. VP4, the larger major structural protein of HRPV-1, forms glycosylated spikes on the virion surface and VP3, the smaller major structural protein, resides on the inner surface of the membrane vesicle. Together, these proteins organize the structure of the membrane vesicle. Quantitative lipid comparison of HRPV-1 and its host Halorubrum sp. revealed that HRPV-1 acquires lipids nonselectively from the host cell membrane, which is typical of pleomorphic enveloped viruses.

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Toxic effects of certain carbon nanomaterials (CNM) have been observed in several exposure scenarios both in vivo and in vitro. However, most of the data currently available has been generated in a high‐dose/acute exposure setup, limiting the understanding of their immunomodulatory mechanisms. Here, macrophage‐like THP‐1 cells, exposed to ten different CNM for 48 h in low‐cytotoxic concentration of 10 µg mL−1, are characterized by secretion of different cytokines and global transcriptional changes. Subsequently, the relationships between cytokine secretion and transcriptional patterns are modeled, highlighting specific pathways related to alternative macrophage activation. Finally, time‐ and dose‐dependent activation of transcription and secretion of M1 marker genes IL‐1β and tumor necrosis factor, and M2 marker genes IL‐10 and CSF1 is confirmed among the three most responsive CNM, with concentrations of 5, 10, and 20 µg mL−1 at 24, 48, and 72 h of exposure. These results underline CNM effects on the formation of cell microenvironment and gene expression leading to specific patterns of macrophage polarization. Taken together, these findings imply that, instead of a high and toxic CNM dose, a sub‐lethal dose in controlled exposure setup can be utilized to alter the cell microenvironment and program antigen presenting cells, with fascinating implications for novel therapeutic strategies.