COVID-19 and nanomaterial airway exposures - comparable consequences?
A major theme in nanosafety concerns the assessment of pulmonary fibrosis as a possible long-term effect of nanomaterial exposure. Acute responses and pulmonary changes occurring both in Covid-19 disease and nanomaterial exposure are strikingly similar. Therefore, nanotoxicology can help to understand the molecular and cellular events behind the Covid-19 disease. For this, we systematically compared the various similarities of the adverse outcomes at cellular, tissue and molecular level between Covid-19 pathogenesis and nanomaterial exposures.
During SARS-CoV-2 infection, the round tip-shaped spike protein binds to the angiotensin converting enzyme II (ACE2) receptor on the surface of target cells. Comparably, one-dimensional nanomaterials similar in size enter the cell by tip recognition and some are even shown to bind ACE2. After internalization, viral particles as well as nanoparticles can escape the endo-lysosomal intracellular compartment leading to lysosomal leakage and generation of reactive oxygen species (ROS). Subsequently, SARS-CoV-2 infection leads to the production of inflammatory mediators and, in severe cases, also pneumocytes hyperplasia, multinucleated giant cell formation, and fibrin clusters, as also detected in the pulmonary tissue after some nanomaterials exposure. Interstitial fibrosis and granulomas have been observed consequently to inhalation of biopersistent, fibrous nanoparticles. In fact, recent evidence from Covid-19 patients has highlighted initial signs of possible pulmonary fibrosis already shortly after disease onset. For this, interdisciplinary approaches and adverse outcome pathway (AOP) development can shed light on possible long term consequences of Covid-19 and can further help to deploy more effective therapies and management strategies.