Antibiotic causes suicide of the bacteria

Researchers discover a method that drives bacteria to suicide

23/03/2011

Not least because many pathogens are now immune to common antibiotics, research on the treatment of bacterial infections is currently in full swing. A promising approach that science is pursuing is to drive bacteria into "suicide" with their own poisons.

The research team led by Anton Meinhart from the Max Planck Institute for Medical Research in Heidelberg has found out how the self-produced poisons of the bacteria work and under what circumstances this leads to the suicide of the bacteria. The scientists hope to be able to use their findings in the future for effective control of dangerous pathogens.

Zeta toxins cause suicide of the bacteria
Numerous dangerous bacteria contain so-called zeta toxins, which lead under certain conditions to the death of the pathogens. In unfavorable living conditions, division-active cells use the self-produced poisons to commit suicide to secure the food base for the remaining dormant pathogens and thus the long-term survival of the bacterial community. This phenomenon, which can almost be called altruism, is triggered by the so-called zeta toxins as soon as the antidotes, which are also contained in the bacteria, lose their function. When this is the case and how the process is done exactly, but was so far unclear. However, the researchers from Heidelberg have now discovered how the suicide poisons found in many dangerous types of bacteria (for example, in the pathogens of pneumonia or blood poisoning) act. The zeta toxins are thus produced as an enzyme continuously by the bacteria themselves, but their effect is offset by a special antidote. In stress situations such as food shortages, the production of the antidote is reduced and the zeta toxins trigger programmed cell death, the so-called apoptosis.

Bacteria burst during cell division
The researchers from Heidelberg were also able to clarify how zeta toxins cause cell division suicide: Zeta toxin causes the formation of the molecule UNAG-3P. This prevents the formation of a new cell wall in the cell division for the separation of the two daughter cells and thus leads to the bursting of the cells. As part of their investigations, the researchers from Heidelberg have tested the effect of a zeta toxin, which they isolated from the causative agent of pneumonia (Streptococcus pneumonia), on the bacterium Echerichia coli. The latter is often used as a human gut bacterium in laboratory research as a model organism for experiments and has no own antidotes. The investigation has shown that the zeta toxins lead to the bursting of bacterial cells during cell division, report the Heidelberg scientists in the latest issue of the journal „PLoS Biology“.

Research approach for the development of a broad-spectrum antibiotic
Particularly interesting for science is the effect of the molecule UNAG-3P, whose production is triggered by the zeta toxins. Because UNAG-3P starts in the critical process of cell division and could be used in the fight against most bacterial infections, so the hope of the Heidelberg researchers. If it were possible to turn UNAG-3P into a drug, this could serve as a broad-spectrum antibiotic in the treatment of many infectious diseases, scientists from the Max Planck Institute believe. However, the programmed suicide of the bacteria may also be achieved by reducing the antidotes. Researchers at the Washington University in St. Louis have recently achieved significant success in eliminating the antidote of a dangerous bacterium with the help of a new drug. Both approaches - the elimination of the antidote and the use of the molecule UNAG-3P - represent a new level of bacterial control that, unlike previous antibiotics, is likely to be at a much lower risk of resistance as the bacteria most likely will not become immune to their own toxins , However, it will take some time for the new methods to become available as drugs, and more comprehensive studies are needed to analyze the process leading to the suicide of the bacteria. (Fp)

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Picture: Ernst Rose