Environmental pollution is one of the major problems affecting the global population health. Car exhausts containing carbon particles, smoking and simply inhalation of dust of various origins for a long time have been recognised as risk factors causing chronic inflammation in the lungs.
It has also been established by now that smoking or exposure to silica-containing dust can both trigger undesirable immune reactions in human organism leading to the development of the so-called autoimmune diseases, such as for example rheumatoid arthritis, affecting and frequently incapacitating millions of people worldwide. Recently, new concerns have been raised associated with the emerging products of nanotechnology which, if not handled appropriately, may contribute to generation of new types of airborne pollutants. Therefore, the importance of identification of possible risks and hazards involved in the manufacturing and use of nanomaterials can't be overestimated.
The researchers of the Nanomedicine and Molecular Imaging team, Trinity College Dublin School of Medicine led by Prof. Yuri Volkov, have decided to investigate if there was a common underlying mechanism contributing to the development of autoimmune diseases operating at the level of human cells following their exposure to nanoparticles of different nature and possessing diverse physical and chemical properties. In their quest for the answer, the scientists applied a wide range of nanomaterials including ultra-fine carbon black, carbon nanotubes and silicon dioxide particles of different sizes, ranging from 20 to 400 nanometres, to human cells derived from the lining of the airway passages and to the cells of phagocytic origin, i.e. those cells which are most frequently exposed to the inhaled foreign particles or which are specialised to engulf and clean up our body from them. At the same time, collaborating researchers from the Health Effects Laboratory Division, National Ins titute for Occupational Safety & Health (Morgantown, WV, USA) have conducted the studies in mice exposed to chronic inhalation of air contaminated with single walled carbon nanotubes.
The result was clear and convincing: all types of nanoparticles under study were causing an identical response in human cells and in the lungs of mice, manifesting in the specific transformation of the amino acid arginine into the molecule called citrulline. Human proteins which incorporate this modified amino acid as building blocks, can no longer function properly and are subject to destruction and elimination by the bodily defence system. Once programmed to get rid of citrullinated proteins, the immune system can start attacking its own tissues and organs, thereby causing the autoimmune processes which may result in rheumatoid arthritis.
It is entirely feasible that some of the human diseases of the same group with a previously uncertain origin may be triggered by the exposure of susceptible individuals to the ultra-small objects presented to us in the air which we breathe or smoke. Preventing or interfering with the resulting citrullination process looks therefore as a p romising target for the development of future preventative and therapeutic approaches in rheumatoid arthritis and possibly other autoimmune conditions.
These data appeared in the journal Nanomedicine (Future Medicine journals group) as a paper "Citrullination of proteins: a common post-translational modification pathway induced by different nanoparticles in vitro and in vivo".
Fonte: Nanoacademia
