Los antibiotics are medicines used to prevent and treat bacterial infections. But in recent years, the abuse of these drugs has caused bacteria to mutate and become more resistant, posing a global threat to public health.
Although non-antibiotic drugs occupy 95% of the drug market, their impact on the emergence and spread of antibiotic resistance remains unclear. A new study from the University of Queensland, published in the journal PNAS, has shown that antidepressantsone of the most frequently prescribed drugs, can also induce antibiotic resistance and persistence.
Antidepressants are consumed in large quantities, with a similar pharmaceutical market share (4.8%) to that of antibiotics (5%). Although it is recognized that antibiotics are the main driver of the increase in antibiotic resistance, little attention is paid to the contribution of antidepressants in this process.
Specifically, research has shown how five of these commonly used drugs (sertraline, escitalopram, bupropion, duloxetine and agomelatine) are capable of generating resistance to a large number of antibiotics in E. coli bacteria. To do this, they cultured strains of this bacterium and subjected them to these antidepressants for 60 days.
According to this new research, antidepressants at clinically relevant concentrations induce resistance to multiple antibiotics, even after short periods of exposure.
Mathematical models also predicted that antidepressants would accelerate the emergence of antibiotic-resistant bacteria and that persistent cells would help maintain resistance. “Overall, our findings highlight the resistance risk to antibiotics caused by antidepressants,” the researchers note.
“In recent years, various evidences have been shown on how non-antimicrobial drugs such as non-steroidal anti-inflammatory drugs, mucolytics such as N-acetylcysteine or even artificial sweeteners such as saccharin can alter bacterial mutagenesis. This work provides new data in this regard”, explains José Manuel Rodríguez Martínez, professor of Microbiology at the University of Seville in statements to SMC Spain.
For this study, a model with laboratory strains has been used in which therapeutic or environmental concentrations of different antidepressants have been used. “These results must be valued accordingly and must be endorsed by additional trials to understand the consequences derived in real life,” explains José Manuel Rodríguez Martínez. “It would be necessary to design trials in patients for clinical validation of these findings,” he adds.