Abstract
Original language | English |
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Pages (from-to) | 38-43 |
Number of pages | 6 |
Journal | BBA - Biomembranes |
Volume | 1515 |
Issue number | 1 |
DOIs | |
Publication status | Published - Nov 2001 |
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Keywords
- Food poisoning
- Pore-forming toxin
- Planar lipid bilayer
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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 -