Differential viability response of prokaryotes and eukaryotes to high strength pulsed magnetic stimuli

• A 60–70% loss in bacterial viability was observed after PMF exposure in vitro.
• A 2–5 fold increase in ROS levels in prokaryotes promoted bacterial death/injury.
• Longer doubling times for the PMF exposed bacterial populations were recorded.
• Eukaryotes exhibited strong antioxidant response leading to their better survival.
• An analytical model for the differential viability response to PMF is proposed.

The present study examines the efficacy of a high strength pulsed magnetic field (PMF) towards bacterial inactivation in vitro, without compromising eukaryotic cell viability. The differential response of prokaryotes [Staphylococcus aureus (MRSA), Staphylococcus epidermidis, and Escherichia coli], and eukaryotes [C2C12 mouse myoblasts and human mesenchymal stem cells, hMSCs] upon exposure to varying PMF stimuli (1–4 T, 30 pulses, 40 ms pulse duration) is investigated.Among the prokaryotes, ~ 60% and ~ 70% reduction was recorded in the survival of staphylococcal species and E. coli, respectively at 4 T PMF as evaluated by colony forming unit (CFU) analysis and flow cytometry. A 2–5 fold increase in intracellular ROS (reactive oxygen species) levels suggests oxidative stress as the key mediator in PMF induced bacterial death/injury. The 4 T PMF treated staphylococci also exhibited longer doubling times. Both TEM and fluorescence microscopy revealed compromised membranes of PMF exposed bacteria. Under similar PMF exposure conditions, no immediate cytotoxicity was recorded in C2C12 mouse myoblasts and hMSCs, which can be attributed to the robust resistance towards oxidative stress. The ion interference of iron containing bacterial proteins is invoked to analytically explain the PMF induced ROS accumulation in prokaryotes. Overall, this study establishes the potential of PMF as a bactericidal method without affecting eukaryotic viability. This non-invasive stimulation protocol coupled with antimicrobial agents can be integrated as a potential methodology for the localized treatment of prosthetic infections.

(a) Proposed mechanism of PMF that induced inner membrane permeabilization mediated by ROS leading to loss of the membrane integrity of the bacterial cell. (b) Schematic diagram showing the absence of cytotoxicity of high strength PMF towards mammalian cells.Figure optionsDownload as PowerPoint slide