Animals have several built-in ways to defend themselves against infection. A new study by FMI researchers and their collaborators at the University of Queensland in Australia points to an unexpected player in that defense: mitochondria, the tiny structures best known for helping cells produce energy.

Researchers led by Ronan Kapetanovic, a former postdoctoral fellow in the lab of emeritus group leader Patrick Matthias, studied macrophages, immune cells that engulf and destroy bacteria.

When macrophages encountered the bacterium Escherichia coli, their mitochondria their mitochondria underwent mitochondrial fission — a normal process in which mitochondria divide into smaller pieces. This splitting helped the cells clear the bacteria. The same response also appeared in the worm Caenorhabditis elegans, suggesting that the defense mechanism is evolutionarily old.

The team found that mitochondrial fission set off two antibacterial responses. One was a stress-response program that helps mitochondria cope with damage. The other was the production of tiny fat-rich structures that can support immune defense.

The enzyme HDAC6, which Matthias’ group has studied for many years, normally kept mitochondria from splitting in response to infection, the researchers found. When they blocked HDAC6, the mitochondria split more readily, and mice cleared the bacteria more effectively.

The findings suggest that influencing the dynamics of mitochondrial shape may be a useful target for future strategies to fight infections, the researchers say.