Shifting identities of metal oxide nanoparticles: Focus on inflammation
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troduction Most formal definitions of engineered nanomaterials revolve around the manipulation of materials roughly 1 to 100 nm in size. Alternative ways of defining nanotechnology focus instead on the novel properties of the particles owing to the small size and not on an exact and/or arbitrary specification of size.1,2 Nanotoxicology, in turn, may be viewed as the study of the interaction or interference of engineered nanomaterials with biological systems at the nano-scale.3 To give an example, Setyawati et al. reported that TiO2 nanoparticles (NPs) caused endothelial cell leakiness through physical (size-dependent) interference with so-called adherens junction complexes, involved in intercellular signaling, thereby disrupting cell–cell interactions.4 Furthermore, due to their small size, NPs can reach places in the body distal to the portal of entry. Hence, small particles can travel deeper into the lungs upon inhalation compared to larger particles. Due to their non-degradability, metal-based NPs specifically can be retained for a long time in the lungs or may translocate to secondary organs by breaching the air-blood barrier and entering systemic circulation.5 This is not seen for larger particles. As pointed out by Kreyling et al., the binding of biomolecules to NPs also plays a key role in translocation of NPs across cellular membranes and organ barriers.6 Thus, the small size confers properties to NPs not seen for larger particles, and this can give rise to unexpected toxicities (i.e., not anticipated from studies of
larger particles), but this also suggests novel applications of NPs in medicine. Inflammation is an adaptive response involving cells and soluble factors—cytokines, chemokines, and others—that is triggered in response to infection, trauma, or other (toxic) insults.7 The cardinal signs of inflammation are redness, heat, pain, and swelling. The process normally leads to recovery of tissue function and healing. However, inflammation can also lead to persistent tissue damage. Inflammation is therefore a double-edged sword. The most important inflammatory cells are monocytes-macrophages, neutrophils, eosinophils, and mast cells, all of which have been implicated in responses to various NPs.7 The purpose of the inflammatory response is to remove or sequester the offending agent, to allow the host to adapt, and, ultimately, to restore functionality to the tissues. If the process becomes chronic, the adaptive changes may become detrimental.8 Thus, it is important to distinguish between transient, protective responses versus chronic and maladaptive ones. This article considers the synthetic versus biological “identity” of NPs and the possibility that these identities may undergo dynamic changes in a living system, through the adsorption and removal of proteins or lipids on the surface of the NPs, or through intra- or extracellular dissolution of NPs with release of toxic ions or other forms of biotransformation. We also discuss the inflammogenic potential of oxide NPs;
Kunal Bhattacharya, Nanosafety and Nanomedici
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