For such simple organisms, bacteria are surprisingly crafty when it comes to defending themselves from antibiotics. They build biofilms to protect colonies, hibernate until the danger passes, and of course they're steadily evolving genetic resistance to our best drugs. Now researchers at Princeton and California State University-Northridge have discovered a new bacterial defense mechanism, where dying bugs will "hoard" antibiotics to allow their neighbors to grow unharmed.
The researchers made the discovery by exposing a colony of E. coli to an antimicrobial peptide molecule known as LL37, which human skin and some organs naturally produce to ward off external bacteria. In this case, the team modified the molecule so that it glowed green, allowing them to track which bacteria absorbed it and how it spread through the population.
The team found that a relatively small amount of E. coli tended to absorb large amounts of the molecule. While that killed the individual cells, it allowed the rest of the colony to continue spreading and growing. In essence, it was like they were sacrificing themselves for the greater good.
Along with the physical experiments, the researchers developed a mathematical model to explain it. By punching in different amounts of bacteria and different doses of the antimicrobial, the model showed the dead cells were indeed sequestering the molecule away, and while the growth of the surviving bacteria did slow down, it still continued.
"The model provided a physical explanation for how this actually works," says Andrej Košmrlj, co-senior author of the study. "We had a surprising observation that the critical inhibitory concentration of antimicrobial peptides depends on the number of bacteria, and our model was able to explain why this happens."
The researchers still don't have all the answers, but a better understanding of the bacterial defense playbook could help scientists develop new ways to thwart them. That's desperately needed, given that currently we seem to be losing the arms race against them.
"This research opens the doors to a lot of questions that were never asked before," says Sattar Taheri-Araghi, co-senior author of the study. "Our findings have profound implications for the evolution of bacteria — which have been around for billions of years — as well as in medicine for the design and administration of novel antibiotics."
The research was published in the journal eLife.
Source: Princeton University