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A German-Dutch study has gained new insights into a mechanism used by bacteria to defend themselves against antibiotics / Published in ‘PNAS’
Bacteria can defend themselves against antibiotics with the help of an enzyme released by dying cells. That is the conclusion reached by a research group made up of researchers from the Institute for Biological Physics at the University of Cologne and Wageningen University & Research. This discovery helps scientists understand the survival mechanisms of bacteria and, as a result, to improve the effectiveness of antibiotics. The team led by Professor Dr Joachim Krug in Cologne and Professor Dr Arjan de Visser in Wageningen demonstrated that Escherichia coli (E. coli) bacteria are capable of producing an enzyme that chemically breaks down the antibiotic, thereby rendering it ineffective. Since the enzyme is released in particular by dying bacteria, the researchers refer to this as ‘altruistic cell death’, which ensures the survival of the population as a whole. These findings help explain the collective survival mechanisms of bacteria, which, in turn, contribute to improving the effectiveness of existing and future antibiotics. The results were published under the title “Contributions of intra- and extracellular antibiotic degradation to collective β-lactam survival” in the journal Proceedings of the National Academy of Sciences (PNAS). The Research was funded by the German Research Foundation (DFG) as part of the work of the Collaborative Research Centre 1310 ‘Predictability in Evolution’.
The project was prompted by a discovery made by the study’s first author, Dr Rotem Gross (University of Cologne), demonstrating that although bacterial cultures initially die off when exposed to the antibiotic, they eventually recover and continue to grow unhindered. The team investigated two different strains of E. coli bacteria – pathogens responsible for urinary tract infections, among other conditions, as well as for septicaemia and hospital-acquired infections – and their response to the administration of beta-lactams, the most widely used class of antibiotics worldwide. The bacteria produce the enzyme beta-lactamase, which chemically breaks down the antibiotic. As soon as its concentration had fallen below a threshold level as a result of enzymatic activity, the bacterial cultures began to recover. “Therefore, the death of some of the bacteria contributes significantly to the long-term survival of the population as a whole, which can be interpreted as an example of altruistic collective behaviour,” says Joachim Krug.
In addition to the dying bacteria, the surviving bacteria also help to fight off the antibiotic. They, too, produce the enzyme, but it remains inside the cell, where it degrades the absorbed antibiotic. The dying bacteria release the enzyme. This occurs in both E. coli stands under investigation. However, the researchers noted that the extent to which cell death contributes to the reduction of the antibiotic varies considerably between the two E. coli strains studied. This suggests that the strains will also react differently to the administration of beta-lactamase inhibitors, as these are only effective in the culture medium and cannot penetrate intact cells. Beta-lactamase inhibitors are substances designed to circumvent the resistance mechanism of bacteria. A higher level of altruistic cell death therefore makes the population more susceptible to these substances, which are already routinely used to treat infections. Joachim Krug: “We were amazed by the variety of defence mechanisms that the bacteria are able to mobilise even under simple laboratory conditions.” This makes predicting the efficacy of specific antibiotics under realistic physiological conditions a major challenge, a task the team hopes to tackle in the future.
Professor Dr Joachim Krug
Institute for Biological Physics
+49 221 470 2818
jkrug@uni-koeln.de
https://www.pnas.org/doi/full/10.1073/pnas.2526410123
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