Depolarization of the Membrane Potential by β-Lactams as a Signal to Induce Autolysis

Penyige, András; Matkó, János; Deák, Eleonóra; Bodnár, Andrea; Barabás, György

doi:10.1006/bbrc.2001.6317

Cited by 14 publications

(12 citation statements)

References 31 publications

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“…The same phenomenon was observed in Streptomyces griseus, where GD or ␤-lactam antibiotics caused autolysis that occurred as a consequence of a drop in ⌬⌿ (42).…”

Section: Depolarization Of the CM Is Not Sufficient To Initiate Lysissupporting

confidence: 62%

“…Depolarization of the CM in gram-positive bacteria stimulates periplasmic autolysins (peptidoglycan-hydrolyzing enzymes) and subsequent cell lysis (30,42). However, our results demonstrate that ER72M2 cells do not undergo lysis as a consequence of the dissipation of the ⌬⌿, since treatment with either GD or KCN did not result in decreased culture turbidity ( Fig.…”

Section: Discussionmentioning

confidence: 65%

See 1 more Smart Citation

Polymyxin B Induces Lysis of Marine Pseudoalteromonads

Krupovìč

Daugelavičius

Bamford

2007

Antimicrob Agents Chemother

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Polymyxin B (PMB) is a cationic antibiotic that interacts with the envelopes of gram-negative bacterial cells. The therapeutic use of PMB was abandoned for a long time due to its undesirable side effects; however, the spread of resistance to currently used antibiotics has forced the reevaluation of PMB for clinical use. Previous studies have used enteric bacteria to examine the mode of PMB action, resulting in a somewhat limited understanding of this process. This study examined the effects of PMB on marine pseudoalteromonads and demonstrates that the frequently accepted view that "what is true for Escherichia coli is true for all bacteria" does not hold true. We show here that in contrast to the growth inhibition observed for enteric bacteria, PMB induces lysis of pseudoalteromonads, which is not prevented by high concentrations of divalent cations. Furthermore, we demonstrate that a high membrane voltage is required for the interaction of PMB with the cytoplasmic membranes of pseudoalteromonads, further elucidating the mechanisms by which PMB interacts with the cell envelopes of those gram-negative bacteria.

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“…The same phenomenon was observed in Streptomyces griseus, where GD or ␤-lactam antibiotics caused autolysis that occurred as a consequence of a drop in ⌬⌿ (42).…”

Section: Depolarization Of the CM Is Not Sufficient To Initiate Lysissupporting

confidence: 62%

Section: Discussionmentioning

confidence: 65%

Polymyxin B Induces Lysis of Marine Pseudoalteromonads

Krupovìč

Daugelavičius

Bamford

2007

Antimicrob Agents Chemother

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“…Membrane depolarization by ␣-MSH-based antimicrobial peptides. Previous studies have reported that various membrane-targeting antimicrobial peptides, such as nisin LL-37, human neutrophil peptide-1 (HNP-1), and gramicidin D, also result in membrane depolarization (19,34,43). In order to analyze whether ␣-MSH and its C-terminal fragments cause membrane depolarization, peptide-treated S. aureus cells were incubated with the membrane potential-sensitive dye DiBAC 4 (3) and compared with untreated control cells.…”

Section: Resultsmentioning

confidence: 99%

C-Terminal Amino Acids of Alpha-Melanocyte-Stimulating Hormone Are Requisite for Its Antibacterial Activity against Staphylococcus aureus

Singh

Mukhopadhyay

2011

Antimicrob Agents Chemother

105

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Alpha-melanocyte-stimulating hormone (␣-MSH) is an endogenous neuropeptide that is known for its anti-inflammatory and antipyretic activities.We recently demonstrated that ␣-MSH possesses staphylocidal activity and causes bacterial membrane damage. To understand the role of its amino acid sequences in the staphylocidal mechanism, in the present study we investigated the antimicrobial activities of different fragments of ␣-MSH, i.e., ␣-MSH(6-13), ␣-MSH(11-13), and ␣-MSH(1-5), and compared them with that of the entire peptide. Our results showed that peptides containing the C-terminal region of ␣-MSH, namely, ␣-MSH(6-13) and ␣-MSH(11-13), efficiently killed >90% of both methicillin-sensitive and -resistant Staphylococcus aureus cells in the micromolar range and ϳ50% of these cells in the nanomolar range; their efficiency was comparable to that of the entire ␣-MSH, whereas the peptide containing the N-terminal region, ␣-MSH(1-5), was found to be ineffective against S. aureus. The antimicrobial activity of ␣-MSH and its C-terminal fragments was not affected by the presence of NaCl or even divalent cations such as Ca 2؉ and Mg 2؉ . Similar to the case for the parent peptide, ␣-MSH(6-13) and ␣-MSH(11-13) also depolarized and permeabilized Staphylococcus cells (ϳ70 to 80% of the cells were depolarized and lysed after 2 h of peptide exposure at micromolar concentrations). Furthermore, scanning and transmission electron microscopy showed remarkable morphological and ultrastructural changes on S. aureus cell surface due to exposure to ␣-MSH-based peptides. Thus, our observations indicate that C-terminal fragments of ␣-MSH retain the antimicrobial activity of entire peptide and that their mechanism of action is similar to that of full-length peptide. These observations are important and are critical in the rational design of ␣-MSH-based therapeutics with optimal efficacy.

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“…Accumulating evidence suggests that the resting membrane potential (RMP) is vital for fulfilling this function. The RMP has been shown to be central to the secretion and synthesis of substances in a variety of other cell types (Breittmayer et al, 1996; McCarty, 1999; Penyige et al, 2002). It therefore seems likely that if the RMP of chondrocytes is changed by ion channel manipulation, their ability to produce ECM will be compromised.…”

Section: Introductionmentioning

confidence: 99%

The emerging chondrocyte channelome

et al. 2010

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Chondrocytes are the resident cells of articular cartilage and are responsible for synthesizing a range of collagenous and non-collagenous extracellular matrix macromolecules. Whilst chondrocytes exist at low densities in the tissue (1–10% of the total tissue volume in mature cartilage) they are extremely active cells and are capable of responding to a range of mechanical and biochemical stimuli. These responses are necessary for the maintenance of viable cartilage and may be compromised in inflammatory diseases such as arthritis. Although chondrocytes are non-excitable cells their plasma membrane contains a rich complement of ion channels. This diverse channelome appears to be as complex as one might expect to find in excitable cells although, in the case of chondrocytes, their functions are far less well understood. The ion channels so far identified in chondrocytes include potassium channels (KATP, BK, Kv, and SK), sodium channels (epithelial sodium channels, voltage activated sodium channels), transient receptor potential calcium or non-selective cation channels and chloride channels. In this review we describe this emerging channelome and discuss the possible functions of a range of chondrocyte ion channels.

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Depolarization of the Membrane Potential by β-Lactams as a Signal to Induce Autolysis

Cited by 14 publications

References 31 publications

Polymyxin B Induces Lysis of Marine Pseudoalteromonads

Polymyxin B Induces Lysis of Marine Pseudoalteromonads

C-Terminal Amino Acids of Alpha-Melanocyte-Stimulating Hormone Are Requisite for Its Antibacterial Activity against Staphylococcus aureus

The emerging chondrocyte channelome

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