Jerusalem Post - The mechanism used by some bacteria to survive antibacterial treatment has been revealed for the first time by Hebrew University of Jerusalem researchers.
The mechanism used by some bacteria to survive antibacterial treatment
has been revealed for the first time by Hebrew University of Jerusalem
researchers. They suggest that their work could pave the way for new
ways to control such pathogens.
In addition to the known phenomenon in which some bacteria achieve
resistance to antibiotics through mutation, there are other types, known
as “persistent bacteria,” that are not resistant to the antibiotics
but simply continue to exist in a dormant or inactive state when
exposed to antibacterial treatment. These bacteria “awaken” when that
treatment is over, resuming their detrimental tasks.
Until now, scientists have been aware of a connection between these
kinds of bacteria and the pathogen’s naturally occurring toxin HipA,
but they didn’t know the cellular target of this toxin and how its
activity triggers dormancy of the bacteria.
Now, the Jerusalem researchers, led by Prof. Gadi Glaser of the faculty
of medicine and Prof. Nathalie Balaban of the Racah Institute of
Physics, have been able to show how this comes about. They demonstrated
that when antibiotics attack these bacteria, the HipA toxin disrupts
the chemical “messaging” process necessary for nutrients to build
proteins. This is interpreted by the bacteria as a “hunger signal” and
sends them into an inactive state (dormancy) in which they are able to
survive until the antibacterial treatment is over.
The research on persistent bacteria has been conducted in Balaban’s lab
for several years, focusing on the development of a biophysical
understanding of the phenomenon.
It will be combined with other work being done in Glaser’s lab that
focuses on fighting persistent bacteria in the hope of leading to more
effective treatment for bacterial infections.
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