Hebrew University research teams
have found how bacteria can survive treatment with antibiotics – even when the
strain is not inherently antibiotic-resistant.
The discovery, which was published
this week in prestigious science journal Nature Communications,
could possibly improve treatment methods for bacterial infections.
Hebrew University’s medical school
and department of developmental biology and cancer research coordinated the
research. Together, they found that while some bacteria mutates to become
resistant to antibiotics, a small percentage also simply becomes “inactive”
during the course of treatment.
The “inactive” bacteria – also
labeled as “persistent bacteria” – then reactivates itself to reinfect
patients, the researchers say.
Until now, it has been known that
there is a relationship between the dormant bacteria and toxin called HipA.
However, the medical world could not determine what chain of actions activates
the toxin, eventually causing some bacteria to sleep and thus evade the effect
of the antibiotics.
Now the study’s authors, Professor
Gadi Glazer of the Faculty of Medicine and Professor Nathalie Balaban of the
Racah Institute of Physics, were able to unravel the mechanism that causes
certain bacteria to “sleep,” so to speak.
The research shows that when the
antibiotics attack the bacteria, the toxin found in the cell prevents the entry
of crucial amino acids – inhibiting protein-building molecules that would allow
the bacteria to leave, researchers say.
Scientists say the information could
provide an entirely new way to treat bacterial infections – through
manipulating the protein output.
Protein and antibiotics have been
linked before. In 2011, a joint project by the research teams at Hebrew
University – Hadassah Medical School and a visiting professor from the
University of Vienna revealed that protein synthesis under stress conditions
affected bacteria. Bacteria which collapsed under “stress conditions” by the
protein synthesis process demonstrated then that antibiotics could use the
process as an alternative mechanism against resistant infections.
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