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Shoo, Fly

Evolutionary biologist Jens Rolff studies the immune systems of insects. His research could inspire human medicine.

Jun 26, 2013

Älter als Dinosaurier: Bei Insekten wirken flexible Eiweißverbindungen gegen Bakterien, Viren und Pilze. Forscher vermuten, dass sie aus diesem Grund in der Evolutionsgeschichte so erfolgreich waren.

Older than dinosaurs: In insects, flexible protein compounds function effectively against bacteria, viruses, and fungi. Researchers suspect that is why insects have been so successful in evolutionary history.
Image Credit: Patrizia Tilly/ Fotolia

Staphylococcus aureus is the name of the invisible enemy in hospitals. The bacterium is actually harmless. It settles on the skin and in the upper airways, where it clusters together like tiny bunches of grapes. Nearly 30 percent of all people in Germany carry the pathogen, and the figure is even higher for nurses and doctors, at about 90 percent. In most cases, S. aureus does not cause any symptoms of disease, but if the host’s immune system is weakened, it attacks the skin, muscles, or airways. That in itself should also be harmless since the discovery of antibiotics. But strains that are resistant to common classes of antibiotics, such as quinolones and tetracyclines, aminoglycosides and sulfonamides, are being found increasingly often in hospital settings. Now, houseflies and honeybees, butterflies and mealworm beetles could help find new methods in the fight against antibiotic-resistant bacteria.

At least 25,000 people die in Europe every year as a result of multiresistant strains of Staphylococcus aureus. By comparison, about 7,000 people now die of AIDS in Central and Western Europe each year.

Jens Rolff, of Freie Universität, is a researcher working on basic research, observing the immune systems of insects. Compared with the complex processes that take place in the human body, a housefly’s defense mechanisms seem modest at first glance. But they are also highly successful: 80 percent of all living animal species on our planet are insects, and they are older than the first dinosaurs, having existed from the Paleozoic period, 450 million years ago.

One thing is clear to Rolff: Without an effective immune system, insects would have gone extinct long ago. “Unlike vertebrates, whose immune system can adapt to intruders and recall pathogens’ strategies, insects’ bodies always have to respond to foreign organisms and substances all over again,” Rolff says.

A crucial role in the process is evidently played by antimicrobial peptides – protein compounds that have a deadly effect on bacteria, viruses, and fungi. Researchers have already detected and identified hundreds of these compounds in insects. Mammals, like humans, also have this kind of immune protection on their skin and mucous membranes.

In his day-to-day work in the lab, Rolff isolates these insect peptides and brings them together with bacteria: “After two weeks at the most, resistant strains of bacteria form in the petri dish. The individual peptide is no longer very effective against them.” Rolff suspects that the bacteria exchange genes with each other, thereby canceling out the peptide’s effects.

And yet, insects in the wild are hardly ever infected with resistant strains of bacteria. Why? In his studies, Rolff has observed that combinations of different peptides keep the bacteria in check: “The insect’s immune system also constantly changes the composition and dosage of the peptides, and it seems to be highly successful that way.” In this mixture, even peptides that have no effect as isolated proteins are effective in fighting germs. “There seems to be an interaction between the various substances,” Rolff says.

Rolff and his team are the first researchers in the world to take this approach. Rolff is currently working with theoreticians from ETH Zurich to pinpoint the dynamics involved in how the peptides kill the bacteria. The question behind it is whether it is possible to predict, based on these germs’ “mortality statistics,” whether and how resistance will arise. Rolff and his team have already made one important finding: While administering an antibiotic increases the mutation rate in bacteria, the rate does not rise when antimicrobial peptides are used. The implication for humans could be that constantly changing concentrations of different antibiotics could help prevent new resistance. Human clinical trials, at any rate, are now showing that this route is very promising.

Further Information

Prof. Dr. Jens Rolff, Freie Universität Berlin, Department of Biology, Chemistry, and Pharmacy, Institute of Biology, Tel.: +49 30 838-54893, Email: jens.rolff@fu-berlin.de