We know how penicillin works. It kills bacteria. But a new study shows that it's not nearly that simple.
Even when it can't kill a bacterium, penicillin forces the cell to kill itself.
Here's how penicillin is supposed to work. It invades a cell, usually a bacterial cell. A cell is constantly engaged in maintaining itself. Its most important defense is its cell wall. To keep the wall strong, it builds long strands of sugar, and links them together to form a barrier. The penicillin takes out an enzyme that helps build the links between the strands of sugar. The cell wall becomes shredded, the cell bursts, and the bacteria dies.
This is why an experiment involving specially engineered E. coli and specially designed penicillin was so odd. The bacteria was engineered so it had that enzyme, but didn't need it to build a good wall. The penicillin was designed only to take out the now-useless enzyme. The study was meant to see what happened in a cell when penicillin couldn't kill it. The bacteria still died. Why?
The study discovered that penicillin and drugs like it work not just because of what they do but because of what they don't do. Penicillin might take out an enzyme that weaves sugar strands into a wall, but it doesn't even remotely stop those strands from being made in the first place. In fact, it might cause the cell to pick up the pace when it comes to making those strands. The strands get made. They're useless. They immediately get broken down again. Then they get made again. The cell throws more and more of its energy into this futile task, until it drains its own resources and dies.
This might open up a new way to combat infections as antibiotics lose their effectiveness. If we can't make drugs to kill cells outright, perhaps we can find other cell mechanisms to exploit.
Top Image: Wellcome Trust