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Polymyxin B and polymyxin B nonapeptide alter cytoplasmic membrane permeability in Escherichia coli
Abstract:
The effects of polymyxin B and polymyxin B nonapeptide (PMBN) on the permeability of the Escherichia coli cytoplasmic membrane were investigated. Both compounds caused loss of free amino acids, uracil and K+ from E. coli. The rates of loss promoted by polymyxin B were one and a half to two-fold greater than those caused by PMBN. Although PMBN mediated loss of low molecular weight substances from E. coli, it was not bactericidal. In contrast, polymyxin B treated E. coli lysed and rapidly lost viability. We suggest that the bactericidal activity of polymyxin B may be related to its previously reported ability to release cytoplasmic proteins from bacteria.
Insights
Polymyxin B and polymyxin B nonapeptide (PMBN) increase Escherichia coli membrane permeability, causing leakage of essential molecules. Polymyxin B is bactericidal, unlike PMBN, suggesting protein release contributes to its killing effect.
Area of Science:
- Microbiology
- Molecular Biology
- Biochemistry
Background:
- Polymyxins are cationic antimicrobial peptides effective against Gram-negative bacteria.
- Understanding their mechanism of action, particularly membrane interactions, is crucial for combating antibiotic resistance.
Purpose of the Study:
- To investigate and compare the effects of polymyxin B and polymyxin B nonapeptide (PMBN) on Escherichia coli cytoplasmic membrane permeability.
- To elucidate the relationship between membrane permeability changes and bacterial viability.
Main Methods:
- Treatment of E. coli with polymyxin B and PMBN.
- Measurement of leakage of intracellular components (amino acids, uracil, K+).
- Assessment of bacterial viability and lysis.
Main Results:
- Both polymyxin B and PMBN induced the loss of intracellular substances from E. coli.
- Polymyxin B promoted faster leakage rates (1.5-2 fold) compared to PMBN.
- PMBN did not exhibit bactericidal activity, whereas polymyxin B caused rapid cell lysis and loss of viability.
Conclusions:
- Polymyxin B's potent bactericidal activity may stem from its ability to induce significant membrane damage and release cytoplasmic proteins.
- PMBN, while affecting membrane permeability, lacks the strong bactericidal effect of polymyxin B, indicating a differential mechanism or threshold for cell death.