2024-07-24 12:18:58
Given the growing threat posed by antibiotic resistance, it is increasingly important to develop strategies that prevent the spread of resistant properties among bacteria and also open new ways in the fight against resistant clinical infections. to traditional treatments.
Antibiotic resistance has become a major threat to human health. There is enough scientific evidence to confirm that one of the main contributors to the spread of antibiotic resistance among different bacteria is type 4 secretion systems (T4SS). Although the T4SS of Gram-negative bacteria have been extensively studied, those of Gram-positive bacteria, which account for more than half of all hospital-acquired infections, are unknown.
Accordingly, researchers from the University of Umeå (Sweden) have provided new clues to understand how antibiotic resistance spreads, based on the study of bacteria. Enterococcus faecalis, which often causes hospital-acquired infections and in which, in many cases, antibiotic treatment no longer works because resistance has developed. The research shows how an enzyme breaks down the bacteria’s outer protective layer, the cell wall, thereby facilitating the transfer of antibiotic resistance genes.
A real ‘complex’
Bacteria Enterococcus faecalis, They can also spread resistance through 4 types of systems, T4SS. It is a type of protein complex that acts as a copying machine, allowing properties in the form of genetic material to be transmitted to other bacteria.
As explained in the study, published in the scientific journal ‘mBio’, an important part of the T4SS is the PrgK enzyme, which breaks down the bacterial cell wall and, in this way, facilitates the transfer of properties among bacteria. “We can say that we are adding a piece to the puzzle in understanding how the antibiotic spreads between bacteria,” Ronnie Berntsson, Ph.D. Associate professor at Umeå University and one of the authors of the study.
The enzyme PrgK, which has three parts or domains: LytM, SLT and CHAP, acts, for example, as ‘scissors that cut the bacterial cell wall’. Contrary to what the researchers thought, it turns out that only the SLT area is active, but in a different way than expected. Two other domains, on the other hand, turned out to have an important role in the regulation of the enzyme. The researchers also identified that another T4SS protein, PrgL, binds to PrgK and ensures that it ends up at the right place in the protein machinery.
The study was carried out by combining biochemical analyzes of the protein linked to in vivo functional studies, and was complemented by structural studies of PrgK using both X-ray crystallography and the AlphaFold model.
““The findings are important for continued research into how to prevent T4SS from transferring properties such as antibiotic resistance to other bacteria,” noted, for his part, Prof. Josy ter Beek, scientist at Umeå University. Rev. Ana Mera, a pharmacist. Barcelona
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