For 20 years, scientists around the world have debated whether bacteria sense the drug itself to trigger resistance or whether they sense the impact it has on the cell wall of bacteria.
Most antibiotics work by inhibiting an enzyme but vancomycin binds to cell wall building blocks, causing a weakness in the structure of the cell wall so the cell bursts and dies.
Some scientists believed that bacteria detect the cell wall degradation to trigger resistance. Others argued that bacteria detect the presence of the drug directly.
Wright and his team studied the vancomycin-resistance mechanism in the harmless soil bacteria Streptomyces coelicolor.
The scientists showed that bacteria detect vancomycin itself. They also conducted preliminary experiments that suggest the same mechanism exists in disease causing bacteria.
"We have finally cracked the alarm system used by bacteria, and hopefully new antibiotics can be developed that don't set it off," said Mark Buttner, a study collaborator and senior scientist at the John Innes Centre.
Marc Ouellette, scientific director of the Institute of Infection and Immunity at the Canadian Institutes for Health Research (CIHR), said the research findings shed new light on the antibiotic resistance issue.
"Thousands of Canadians die every year from antibiotic-resistant infections," Ouellette said. "This issue has long been a priority of the CIHR and this exciting work expands our understanding of how bacteria develop resistance to antibiotics. It lays the groundwork for developing new therapies to prevent and treat antibiotic-resistant infections."
|Contact: Susan Emigh|