## Abstract __Clostridium difficile__βassociated disease causes diarrhea to fulminant colitis and death. We investigated the role of phospholipase A~2~ (PLA~2~) inhibitors, aristolochic acid (AA), bromophenacyl bromide (BPB) and quinacrine (QUIN) on the __C. difficile__ toxin Aβinduced disruption o
Activation of cellular phospholipase A2 by Clostridium difficile toxin B
β Scribed by Maria Caspar Shoshan; Inger Florin; Monica Thelestam
- Publisher
- John Wiley and Sons
- Year
- 1993
- Tongue
- English
- Weight
- 860 KB
- Volume
- 52
- Category
- Article
- ISSN
- 0730-2312
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β¦ Synopsis
C difficile toxin B i s a potent cytotoxin known to disrupt the microfilaments of cultured cells We have recently shown also increased phospholipase A2 activity in cells treated with toxin B The activity was detected as a toxin-induced, dose-dependent release of 14C-arachidonic acid from prelabeled fibroblasts Here is shown that the toxin elicited a "T-arachidonic acid release in a cell mutant resistant to the toxin B effect on the microfilaments The toxin-induced release was further characterized usingfibrobldsts. Within 20 min high doses of toxin B (6 pg/ml) elicited a release which increased exponentially with time O f the major membrane phospholipids the lipase activity affected mainly phosphatidyl ethanolamine Neither cycloheximide nor pertussis toxin treatment of target cells inhibited the toxin-induced release, while it could be increased with 12-O-tetradecanoylphorbol-l3-acetate Our results also suggest a toxin-mediated increase in phospholipase C activity occurring at a later stage than the phospholipase A2 activation
We conclude that the ability of toxin B to induce phospholipase activation represents a hitherto unrecognized toxin B effect which is neither a cause nor a consequence of toxin-induced microfilament disorganization 1993 WiIey-Lis inc
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