SARS, avian flu, and other lung diseases destroy the lungs via a common mechanism, researcher report in __Cell__ today. That mechanism, based on innate immunity, could provide new targets for treating severe lung damage, the linkurl:researchers say.; Joseph Penninger, from the Institute of Molecular Biotechnology of the Austrian Academy of Sciences, and colleagues set up an intensive care unit for mice in his lab in order to study lung failure. They intubated knockout mice and monitored oxygen pressure and tidal volume. Only one mouse, lacking a functioning toll-like receptor 4 (TLR-4), showed a decrease in lung damage. TLR-4 is an important receptor in innate immunity, which signals activation via two pathways, TRIF and MyD88. The researchers found that lung injury was mediated exclusively through the TRIF pathway and not via MyD88. Also, the trigger for TLR-4 turned out to be the oxidation of the animals' own lung surfactant, made up...

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