New study discovers why "persister" cells never say die
NU biologist isolates gene making infections drug-resistant
Northeastern University today announced that biologist Kim Lewis has discovered the gene that prevents antibiotics from successfully destroying infections within biofilm. For years, scientists have struggled to understand why a certain type of infection – known as biofilms – are often resistant to antibiotics. Biofilms contain cells that are identical to the infecting cells, but are not corrupted and destroyed by antibiotics. Lewis discovered these “persister” cells, contain a gene (HipA) that generates a toxin (the ReIE toxin) which puts the cell into hibernation and because antibiotics must work on growing cells to destroy them, the hibernating cells can outlast the antibiotic and then repopulate the infection.
The results of the study appears in the most recent issue of the Journal of Bacteriology, titled “Specialized Persister Cells and the Mechanism of Multidrug Tolerance in Escherichia coli.” Lewis, the lead author, worked with NU graduate students Iris Keren, Devang Shaw and Amy Spoering , as well as Niilo Kaldalu of Tartu University in Estonia. “ The implications for the discovery are significant; medical science is racing the clock against increasingly drug-tolerant infections. Biofilm infections are notoriously difficult to stamp out. Armed with the knowledge of the HipA gene that allows the infections to persist, sometime for years, biologists can look for ways to deactivate the gene and wipe out the infection,” says Lewis.
Biofilm infections, which attach to a surface while encased in a membrane, typically attack surgically implanted medical devices, such as mechanical heart valves or artificial joints. They can also take the form of periodontal disease, ear infections or fatal lung infections. The infection can be nearly impossible to eradicate, requiring implants to be removed at great risk and cost. Deleting or deactivating the HipA gene could save thousands of lives and millions of dollars.
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