Most antimicrobial peptides (AMPs) induce membrane damage such as pore formation in bacterial cells, resulting in rapid cell death. On the other hand, bacterial cells have a large intracellular turgor pressure, i.e., an osmotic pressure (Π) due to higher osmolarity inside bacterial cells, but the effects of Π on the membrane permeation of the internal contents of lipid vesicles and cells through AMP-induced pores are unknown. Here, we investigated the effect of Π on the membrane permeability of a water-soluble fluorescent probe, AlexaFluor 488 hydrazide (AF488), when passing through peptidyl-glycylleucine-carboxyamide (PGLa)- or magainin 2 (Mag)-induced nanopores in giant unilamellar vesicles (GUVs). For the interaction of PGLa with single GUVs under Π, the onset of pore formation was followed by a gradual increase in the membrane permeability coefficient, MP, until MP reached a steady value, Ps. On the other hand, for the interaction of Mag with single GUVs under Π, the onset of pore formation was rapidly followed by a change of MP to Ps. Small Π values enhanced the Ps values of AF488 passing through the PGLa- or Mag-induced nanopores. The mechanisms underlying the increase of Ps at small Π values were discussed. Based on these results and our previous results that the membrane tension (due to Π) enhances rate of AMP-induced pore formation, we consider the role of turgor pressure in AMP-induced damage in bacterial membranes and the efflux of internal contents.
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