Researchers at the Hebrew University of Jerusalem said that they have made a major breakthrough in deciphering the mechanism by which some bacteria are able to survive antibacterial treatment.
While some bacteria achieve resistance to antibiotics through mutation, other types, known as "persistent bacteria," continue to exist in a dormant state while exposed to medication, and resume their detrimental activity when the treatment is over.
Scientists have identified the villain as the bacteria's naturally occurring toxin HipA, but so far have been unable to explain how it triggers the inactive state.
A lengthy study led by Gadi Glaser, a professor at Hebrew University's Faculty of Medicine, and Nathalie Balaban, a professor at the Racah Institute of Physics, has revealed 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 in which they are able to weather the treatment, the university said in a statement released Sunday.
The project, conducted in Prof. Balaban's lab for several years by PhD candidates Eitan Rotem and Noga Weiss, focused on developing a biophysical understanding of the mechanism.
The researchers now hope their discovery will pave the way for more effective ways to combat bacterial infections, the statement said.
Sunday, December 29, 2013
Israeli researchers crack mechanism behind persistent bacteria
Researchers at the Hebrew University of Jerusalem said that they have made a major breakthrough in deciphering the mechanism by which some bacteria are able to survive antibacterial treatment.
While some bacteria achieve resistance to antibiotics through mutation, other types, known as "persistent bacteria," continue to exist in a dormant state while exposed to medication, and resume their detrimental activity when the treatment is over.
Scientists have identified the villain as the bacteria's naturally occurring toxin HipA, but so far have been unable to explain how it triggers the inactive state.
A lengthy study led by Gadi Glaser, a professor at Hebrew University's Faculty of Medicine, and Nathalie Balaban, a professor at the Racah Institute of Physics, has revealed 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 in which they are able to weather the treatment, the university said in a statement released Sunday.
The project, conducted in Prof. Balaban's lab for several years by PhD candidates Eitan Rotem and Noga Weiss, focused on developing a biophysical understanding of the mechanism.
The researchers now hope their discovery will pave the way for more effective ways to combat bacterial infections, the statement said.
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