The Spanish flu outbreak of 1918 killed between 30 and 50 million people. In the infected patients, the ultimate cause of death was acute respiratory distress syndrome (ARDS). This fatal condition is a massive reaction of the body during which the lung becomes severely damaged. ARDS can be induced by various bacterial and viral infections, but also by chemical agents. These could be toxic gases that are inhaled or gastric acid when aspirated. Once ARDS has developed, survival rates drop dramatically. Among patients infected with H5N1 bird flu, about 50 percent die of ARDS.
An international team of scientists has been addressing the underlying disease mechanisms for the past five years. The team involved researchers from leading institutions in Vienna, Stockholm, Cologne, Beijing, Hongkong, and Toronto as well as the US-army at Fort Detrick. The international effort was coordinated by Josef Penninger and Yumiko Imai of the Institute of Molecular Biotechnology (IMBA) of the Austrian Academy of Sciences.
A first breakthrough came in 2005 when IMBA-scientists identified ACE2 as the essential receptor for SARS virus infections and showed that ACE2 can protect from acute lung failure in disease models (Imai et al. Nature 2005; Kuba et al. Nature Medicine 2005). Based on these data, ACE2 is now under therapeutic development.
In a paper published by Cell this week, the authors describe an essential key injury pathway that is operational in multiple lung injuries and directly links oxidative stress to innate immunity. They also report for the first time a common molecular disease pathway explaining how diverse non-infectious and infectious agents such as anthrax, lung plague, SARS, and H5N1 avian influenza may cause severe and often lethal lung failure with similar pathologies.
To identify these pathways, the researchers studied numerous tissue samples from deceased humans and animals. Victims of bird flu and SARS were examined in Ho
|Contact: Dr. Heidemarie Hurtl|
Research Institute of Molecular Pathology