Years of research into inflammatory disease, costing billions of dollars in research funding, has been wasted on the lowly mouse.
To assess the mouse as a model for inflammation, the authors performed all the procedures described above and analyzed the animals' white blood cells for changes in the activity of their genes. Then they did the same for human patients, by comparing blood-cell samples drawn from healthy people to those from people suffering from the analogous diseases (inflammation brought on by burns or trauma, or in some experimental conditions, by injection with the endotoxin). Finally, the scientists placed the mouse and human data side by side. How similar, in fact, were the genes involved in each species' inflammation? Which molecules or kinds of signaling inside a cell did these two systems share?Yes, that explains a whole lot.
The answer: not many. The correlation between mice and people was close to zero. For any given human gene that kicked up its activity or battened down in response to inflammation, there was a 50-50 chance that a corresponding mouse gene would be moving in the same direction.
Will someone please redo this experiment with rats? I thought it was very promising.
