Most medically important antibiotics come from soil bacteria. Conventional wisdom holds that dirt microbes evolved these compounds as lethal weapons in the fierce battle waged beneath our feet for food and territory. For more than 15 years microbiologist Julian Davies of the University of British Columbia has been arguing otherwise. “They’re talking, not fighting,” Davies says.
His respected if not wholly accepted theory is that bacteria use most of the small molecules we call antibiotics for communication. As evidence, Davies points out that in nature, soil bacteria secrete antibiotics at trace levels that do not come close to killing their microbial neighbors. “Only when we use them at unnaturally high concentrations do we find that these chemicals inhibit bacteria,” he explains.
Moreover, in Davies’s Vancouver laboratory, his staff has been eavesdropping on the flurry of gene activity in bacteria exposed to low-dose antibiotics. The researchers equip their bacteria with glow-in-the-dark lux genes that provide a fluorescent signal when other linked genes are active; then they watch those genetic “switchboards” light up in a chorus of responses to antibiotic exposure. The call-and-response activity resembles that of cells responding to hormones, Davies observes, or of “quorum-sensing” bacteria that assess their own numbers.
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“I’m not saying that some of these compounds couldn’t be used as weapons in nature,” Davies says. “But that’s not what we’re seeing.” He notes that a gram of soil contains more than 1,000 different types of bacteria. “They’re all thriving there together and clearly not killing one another.” Davies proposes that many antibiotics may help coordinate bacterial activities such as swarming, biofilm formation and diverse interactions with their multicellular hosts.
Davies’s theory implies both good news and bad for the world of medicine. Bacterial communities (and not just those in dirt) might be treasure troves of chemicals with microbe-killing drug potential. Davies and his colleagues have already found candidate molecules among gut bacteria such as Escherichia coli. But for every new antibiotic, there may also already be plenty of corresponding resistance genes. After all, the same bacteria that regularly produce and respond to antibiotics need mechanisms for protecting themselves from potentially toxic effects. And in the gene-swapping world of bacteria, it doesn’t take long for such DNA instructions to jump from one species to many once a new antibiotic comes into widespread medical use.
