Our overall hypothesis is that exposure to antibiotics, in particular at lower concentrations, will initiate bacterial stress. Such stress will induce bacteriophages capable of transferring antibiotic resistance to sensitive bacteria. This spread, and activation, can in turn be regulated by the commensal microbiota, affecting the perceived stress level. Thus, we postulate that subclinical levels of antibiotics drive spread of resistance through transduction, with the presence of specific microbiota through their effector molecules, mitigate the spread of resistance.
|Gällande start-/slutdatum||2022/08/01 → 2023/06/30|
- Crafoordska stiftelsen