In recent years, a body of publications in the microbiology field has challenged all previous knowledge of how antibiotics kill bacteria. "A slew of papers came out studying this phenomenon, suggesting that there is a general mechanism of killing by antibiotics," said Kim Lewis, Northeastern University Distinguished Professor in the Department of Biology and director of Northeastern's Antimicrobial Discovery Center.
The standard thinking at the time was that the three main classes of bactericidal antibiotics each had a unique way of killing bacterial cellslike specialized assassins each trained in a single type of weaponry. But this new research suggested that all antibiotics work the same way, by urging bacterial cells to make compounds called reactive oxygen species, or ROS, which bacteria are naturally susceptible to.
"If they were right it would have been an important finding that could have changed the way we treat patients," said Iris Keren, a senior scientist in Lewis' lab.
And that's exactly how science usually works, said Lewisthrough challenges to mainstream thinking. But recent results reported by Lewis, Keren, and their research partners in an article published Friday in the journal Science suggest that this alternative hypothesis doesn't hold up. For example, even bacteria that are incapable of making ROS are still vulnerable to antibiotics. Further, some antibiotics can work their fatal magic in both aerobic and anaerobic conditionsbut reactive oxygen species can only form when there's oxygen to fuel them.
"We chose to do the simplest and most critical experiment aimed at falsifying this hypothesis," said Lewis. "Killing by antibiotics is unrelated to ROS production," the authors wrote. The findings were corroborated by University of Illinois researchers in another study released on Friday.
The team treated bacterial cultures with antibiotics in both the presence and absence of oxygen. Other tha
|Contact: Lori Lennon|
Northeastern University College of Science