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- W1977892595 abstract "The gene encoding the α-(cpa) is present in all strains of Clostridium perfringens , and the purified α-toxin has been shown to be a zinc-containing phospholipase C enzyme, which is preferentially active towards phosphatidylcholine and sphingomyelin. The α-toxin is haemolytic as a result if its ability to hydrolyse cell membrane phospholipids and this activity distinguishes it from many other related zinc-metallophospholipases C. Recent studies have shown that the α-toxin is the major virulence determinant in cases of gas gangrene, and the toxin might play a role in several other diseases of animals and man as diverse as necrotic enteritis in chickens and Crohn's disease in man. In gas gangrene the toxin appears to have three major roles in the pathogenesis of disease. First, it is able to cause mistrafficking of neutrophils, such that they do not enter infected tissues. Second, the toxin is able to cause vasoconstriction and platelet aggregation which might reduce the blood supply to infected tissues. Finally, the toxin is able to detrimentally modulate host cell metabolism by activating the arachidonic acid cascade and protein kinase C. The molecular structure of the α-toxin reveals a two domain protein. The amino-terminal domain contains the phospholipase C active site which contains zinc ions. The carboxyterminal domain is a paralogue of lipid binding domains found in eukaryotes and appears to bind phospholipids in a calcium-dependent manner. Immunisation with the non-toxic carboxyterminal domain induces protection against the α-toxin and gas gangrene and this polypeptide might be exploited as a vaccine. Other workers have exploited the entire toxin as the basis of an anti-tumour system." @default.
- W1977892595 created "2016-06-24" @default.
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- W1977892595 date "1999-04-01" @default.
- W1977892595 modified "2023-10-18" @default.
- W1977892595 title "The Clostridium perfringensα-toxin" @default.
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- W1977892595 doi "https://doi.org/10.1006/anae.1999.0191" @default.
- W1977892595 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/16887662" @default.
- W1977892595 hasPublicationYear "1999" @default.
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