Clostridium perfringens type A enterotoxin forms mepacrine-sensitive pores in pure phospholipid bilayers in the absence of putative receptor proteins

S.P. Hardy, C. Ritchie, Marcus Allen, R.H. Ashley, P.E. Granum

Research output: Contribution to journal › Article

Abstract

Clostridium perfringens enterotoxin (CPE) is an important cause of food poisoning with no significant homology to other enterotoxins and its mechanism of action remains uncertain. Although CPE has recently been shown to complex with tight junction proteins, we have previously demonstrated that CPE increases ionic permeability in single Caco-2 cells using the whole-cell patch-clamp technique, thereby excluding any paracellular permeability. In this paper we demonstrate that CPE forms pores in synthetic phospholipid membranes in the absence of receptor proteins. The properties of the pores are consistent with CPE-induced permeability changes in Caco-2 cells suggesting that CPE has innate pore-forming ability.
Original languageEnglish
Pages (from-to)38-43
Number of pages6
JournalBBA - Biomembranes
Volume1515
Issue number1
DOIs
Publication statusPublished - Nov 2001

Fingerprint

Quinacrine
Phospholipids
Permeability
Proteins
Caco-2 Cells
Tight Junction Proteins
Foodborne Diseases
Enterotoxins
Patch-Clamp Techniques
Clostridium enterotoxin
Membranes

Keywords

  • Food poisoning
  • Pore-forming toxin
  • Planar lipid bilayer

Cite this

Hardy, S.P. ; Ritchie, C. ; Allen, Marcus ; Ashley, R.H. ; Granum, P.E. / Clostridium perfringens type A enterotoxin forms mepacrine-sensitive pores in pure phospholipid bilayers in the absence of putative receptor proteins. In: BBA - Biomembranes. 2001 ; Vol. 1515, No. 1. pp. 38-43.
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abstract = "Clostridium perfringens enterotoxin (CPE) is an important cause of food poisoning with no significant homology to other enterotoxins and its mechanism of action remains uncertain. Although CPE has recently been shown to complex with tight junction proteins, we have previously demonstrated that CPE increases ionic permeability in single Caco-2 cells using the whole-cell patch-clamp technique, thereby excluding any paracellular permeability. In this paper we demonstrate that CPE forms pores in synthetic phospholipid membranes in the absence of receptor proteins. The properties of the pores are consistent with CPE-induced permeability changes in Caco-2 cells suggesting that CPE has innate pore-forming ability.",
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Hardy, SP, Ritchie, C, Allen, M, Ashley, RH & Granum, PE 2001, 'Clostridium perfringens type A enterotoxin forms mepacrine-sensitive pores in pure phospholipid bilayers in the absence of putative receptor proteins', BBA - Biomembranes, vol. 1515, no. 1, pp. 38-43. https://doi.org/10.1016/S0005-2736(01)00391-1

Clostridium perfringens type A enterotoxin forms mepacrine-sensitive pores in pure phospholipid bilayers in the absence of putative receptor proteins. / Hardy, S.P.; Ritchie, C.; Allen, Marcus; Ashley, R.H.; Granum, P.E.

In: BBA - Biomembranes, Vol. 1515, No. 1, 11.2001, p. 38-43.

Research output: Contribution to journal › Article

TY - JOUR

T1 - Clostridium perfringens type A enterotoxin forms mepacrine-sensitive pores in pure phospholipid bilayers in the absence of putative receptor proteins

AU - Hardy, S.P.

AU - Ritchie, C.

AU - Allen, Marcus

AU - Ashley, R.H.

AU - Granum, P.E.

PY - 2001/11

Y1 - 2001/11

N2 - Clostridium perfringens enterotoxin (CPE) is an important cause of food poisoning with no significant homology to other enterotoxins and its mechanism of action remains uncertain. Although CPE has recently been shown to complex with tight junction proteins, we have previously demonstrated that CPE increases ionic permeability in single Caco-2 cells using the whole-cell patch-clamp technique, thereby excluding any paracellular permeability. In this paper we demonstrate that CPE forms pores in synthetic phospholipid membranes in the absence of receptor proteins. The properties of the pores are consistent with CPE-induced permeability changes in Caco-2 cells suggesting that CPE has innate pore-forming ability.

AB - Clostridium perfringens enterotoxin (CPE) is an important cause of food poisoning with no significant homology to other enterotoxins and its mechanism of action remains uncertain. Although CPE has recently been shown to complex with tight junction proteins, we have previously demonstrated that CPE increases ionic permeability in single Caco-2 cells using the whole-cell patch-clamp technique, thereby excluding any paracellular permeability. In this paper we demonstrate that CPE forms pores in synthetic phospholipid membranes in the absence of receptor proteins. The properties of the pores are consistent with CPE-induced permeability changes in Caco-2 cells suggesting that CPE has innate pore-forming ability.

KW - Food poisoning

KW - Pore-forming toxin

KW - Planar lipid bilayer

U2 - 10.1016/S0005-2736(01)00391-1

DO - 10.1016/S0005-2736(01)00391-1

M3 - Article

VL - 1515

SP - 38

EP - 43

JO - BBA - Biomembranes

JF - BBA - Biomembranes

SN - 0005-2736

IS - 1

ER -

Hardy SP, Ritchie C, Allen M, Ashley RH, Granum PE. Clostridium perfringens type A enterotoxin forms mepacrine-sensitive pores in pure phospholipid bilayers in the absence of putative receptor proteins. BBA - Biomembranes. 2001 Nov;1515(1):38-43. https://doi.org/10.1016/S0005-2736(01)00391-1

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