A review is presented of the literature data concerning the effects induced by carbon nanoparticles on the biological environment and the importance of these effects in human and animal health. The discovery in 1985 of fullerenes, a novel carbon allotrope with a polygonal structure made up solely by 60 carbon atoms, and in 1991 of carbon nanotubes, thin carbon filaments (1–3 μm in length and 1–3 nm in diameter) with extraordinary mechanical properties, opened a wide field of activity in carbon research. During the last few years, practical applications of fullerenes as biological as well as pharmacological agents have been investigated. Various fullerene-based compounds were tested for biological activity, including antiviral, antioxidant, and chemiotactic activities. Nanotubes consist of carbon atoms arranged spirally to form concentric cylinders, that are perfect crystals and thinner than graphite whiskers. They are stronger than steel but very flexible and lightweight and transfer heat better than any other known material. These characteristics make them suitable for various potential applications such as super strong cables and tips for scanning probe microscopes, as well as biomedical devices for drug delivery, medical diagnostic, and therapeutic applications. The effects induced by these nanostructures on rat lung tissues, as well as on human skin and human macrophage and keratinocyte cells are presented.

Nanomaterials and structures, such as nanoparticles, nanofibers, nanosurfaces, nanocoatings, nanoscaffolds and nanocomposites, are considered for various applications in orthopedics and traumatology. This review looks at proposed nanotechnology inspired applications for implants from the perspective of the orthopedic industry. Investigations support consistently the theory that most nanomaterials in various physical forms are able to enhance the cell response selectively for biological tissue integration or increase the strength and wear resistance of current orthopedic materials. At this stage, most of the studies are at the laboratory scale or in early in vivo testing. Significant basic and applied research and development is needed to realize their full clinical potential and biological, manufacturing, economic and regulatory issues have to be addressed. Nevertheless, a crucial factor for success is well-coordinated multimethod and multidiscipline teamwork with profound industrial and medical expertise.

In the last years carbon nanotubes have attracted increasing attention for their potential applications in the biomedical field as diagnostic and therapeutic nano tools. Here we investigate the antimicrobial activity of different fully characterized carbon nanotube types (single walled, double walled and multi walled) on representative pathogen species: Gram-positive Staphylococcus aureus, Gram-negative Pseudomonas aeruginosa and the opportunistic fungus Candida albicans. Our results show that all the carbon nanotube types possess a highly significant antimicrobial capacity, even though they have a colony forming unit capacity and induction of oxidative stress in all the microbial species to a different extent. Moreover, scanning electron microscopy analysis revealed that the microbial cells were wrapped or entrapped by carbon nanotube networks. Our data taken together suggest that the reduced capacity of microbial cells to forming colonies and their oxidative response could be related to the cellular stress induced by the interactions of pathogens with the CNT network.

Diesel exhaust particles (DEP) are major constituents of ambient air pollution and their adverse health effect is an area of intensive investigations. With respect to the immune system, DEP have attracted significant research attention as a factor that could influence allergic diseases interfering with cytokine production and chemokine expression. With this exception, scant data are available on the impact of DEP on lymphocyte homeostasis. Here, the effects of nanoparticles from Euro 4 (E4) and Euro 5 (E5) light duty diesel engines on the phenotype and function of T lymphocytes from healthy donors were evaluated. T lymphocytes were isolated from peripheral blood obtained from healthy volunteers and subsequently stimulated with different concentration (from 0.15 to 60 μg/ml) and at different time points (from 24 h to 9 days) of either E4 or E5 particles. Immunological parameters, including apoptosis, autophagy, proliferation levels, mitochondrial function, expression of activation markers and cytokine production were evaluated by cellular and molecular analyses. DEP exposure caused a pronounced autophagic-lysosomal blockade, thus interfering with a key mechanism involved in the maintaining of T cell homeostasis. Moreover, DEP decreased mitochondrial membrane potential but, unexpectedly, this effect did not result in changes of the apoptosis and/or necrosis levels, as well as of intracellular content of adenosine triphosphate (ATP). Finally, a down-regulation of the expression of the alpha chain of the interleukin (IL)-2 receptor (i.e., the CD25 molecule) as well as an abnormal Th1 cytokine expression profile (i.e., a decrease of IL-2 and interferon (IFN)-γ production) were observed after DEP exposure. No differences between the two compounds were detected in all studied parameters. Overall, our data identify functional and phenotypic T lymphocyte parameters as relevant targets for DEP cytotoxicity, whose impairment could be detrimental, at least in the long run, for human health, favouring the development or the progression of diseases such as autoimmunity and cancer.

Objectives. To evaluate the inflammatory status and the cartilage regenerative potential of pathological synovial fibroblasts from patients with osteoarthritis (OA) compared with non-inflamed synovium (NS)-derived cells from patients with chondropathy. Methods. The inflammatory cell phenotype was investigated based on the constitutive and inducible surface expression and secretion of various effector molecules using flow cytometry or ELISA assays. The capacity of cells to produce cartilage-like extracellular matrix was assessed using acid Alcian blue staining and type II collagen immunostaining after treatment with transforming growth factor β1 (TGF-β1). Results. OA and NS fibroblasts consistently expressed CD29, CD44, CD49e, CD54, CD90 and CD106. Expression of high-affinity receptors for IL-4, IL-15, CXCL8 and CXCL12 was also detected but only intracellularly. All types of fibroblasts spontaneously released abundant amounts of CXCL12, CCL2, IL-6 and tissue inhibitor of metalloproteinase 1, while the production of IL-11, TGF-β1, matrix metalloproteinase 1 (MMP-1) and MMP-9 was detected at moderate levels. Several other secreted factors remained undetectable. No statistically significant differences were noted between the two groups of fibroblasts. Treatment with the proinflammatory cytokine tumour necrosis factor α (TNF-α) up-regulated the same set of surface and secreted molecules, including CD54, CD106, membrane IL-15, CCL2 and CCL5. Under TGF-β1 treatment and adipogenic culture conditions, both OA and NS fibroblasts displayed chondrogenic and adipocytic activities that were reduced in OA compared with NS cells. Conclusions. OA synovial fibroblasts did not display a distinct activated inflammatory phenotype compared with NS cells. However, they did differ in their reduced ability to produce cartilage-like matrix. This difference may be an additional important factor contributing to OA pathogenesis.