The Inflammatory Process in Response to Nanoparticles

Today, numerous nanotechnology-derived applications are commercially available. More than 1000 products are already available on the market [1, 2]. The use of nanoparticles (NPs) has increased in the past few years in various fields including defence, aerospace, electronics, biology, and medicine. Therefore as human exposure to NPs increases, so do investigations on their toxicity. In one hand, nanotoxicology can be seen as an important subdiscipline of toxicology, and, on the other hand, it also represents a subdiscipline of nanotechnology [3]. Studies show that many parameters such as the diameter, surface area, surface composition, and solubility, to name a few, can all have an effect on cell responses, cellular interactions, and reactive oxygen species (ROS) production. They can also have an effect on NP capacity to bind to certain proteins or receptors. More importantly these parameters and others have also the potential to influence an inflammatory response following NP exposure as it has been shown in many in vitro and in vivo studies [4–7]. It has often been demonstrated that smaller particles tend to induce greater inflammatory responses than their bigger counterparts of same chemical composition [5]. Although some NPs may possess proinflammatory activities, the use of others and NP techniques can be very useful in medicine; for example, they can be used for drug-delivery therapies and may also represent excellent biomarkers for the diagnosis of diverse diseases, including inflammatory diseases. In an effort to increase our general knowledge regarding the inflammatory properties of NPs, this special issue of TheScientificWorldJOURNAL was planned in order to generate an important bibliographic tool in this emerging area of research. As the main organ in which the effect of NPs has been (and is still) addressed in the literature is the lung, the first paper from K.-I. Inoue and H. Takano provides insights into the immunotoxicity of airborne and engineered NPs. It deals with the fact that such NPs act as an exacerbating factor on hyper susceptible subjects with immune-mediated pulmonary inflammation. Interestingly, this review put the emphasis on the fact that impairment of both innate and adaptive immunity following NP exposure may synergistically facilitate pathological pulmonary inflammation. The second article is a contribution from M. Roursgaard and collaborators that also focuses on pulmonary inflammation, but by specifically investigating acute and subchronic airway inflammation of quartz and Titanium dioxide (TiO2) agglomerates administered by intratracheal instillation in mice. Inflammation was evaluated from the bronchoalveolar lavage fluids content of inflammatory cells, the cytokines TNF-α, and IL-6 as well as from lung histology. Using this approach, the inflammatory effects