Linked Life Data

10476029

Source:http://linkedlifedata.com/resource/pubmed/id/10476029

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1999-10-21
pubmed:abstractText
Previous epidemiological studies have implicated Clostridium perfringens enterotoxin (CPE) as a virulence factor in the pathogenesis of several gastrointestinal (GI) illnesses caused by C. perfringens type A isolates, including C. perfringens type A food poisoning and non-food-borne GI illnesses, such as antibiotic-associated diarrhoea and sporadic diarrhoea. To further evaluate the importance of CPE in the pathogenesis of these GI diseases, allelic exchange was used to construct cpe knock-out mutants in both SM101 (a derivative of a C. perfringens type A food poisoning isolate carrying a chromosomal cpe gene) and F4969 (a C. perfringens type A non-food-borne GI disease isolate carrying a plasmid-borne cpe gene). Western blot analyses confirmed that neither cpe knock-out mutant could express CPE during either sporulation or vegetative growth, and that this lack of CPE expression could be complemented by transforming these mutants with a recombinant plasmid carrying the wild-type cpe gene. When the virulence of the wild-type, mutant and complementing strains were compared in a rabbit ileal loop model, sporulating (but not vegetative) culture lysates of the wild-type isolates induced significant ileal loop fluid accumulation and intestinal histopathological damage, but neither sporulating nor vegetative culture lysates of the cpe knock-out mutants induced these intestinal effects. However, full sporulation-associated virulence could be restored by complementing these cpe knock-out mutants with a recombinant plasmid carrying the wild-type cpe gene, which confirms that the observed loss of virulence for the cpe knock-out mutants results from the specific inactivation of the cpe gene and the resultant loss of CPE expression. Therefore, in vivo analysis of our isogenic cpe mutants indicates that CPE expression is necessary for these two cpe-positive C. perfringens type A human disease isolates to cause GI effects in the culture lysate:ileal loop model system, a finding that supports CPE as an important virulence factor in GI diseases involving cpe-positive C. perfringens type A isolates.
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0950-382X
pubmed:author
pubmed:issnType
Print
pubmed:volume
33
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
946-58
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:10476029-Animals, pubmed-meshheading:10476029-Bacterial Toxins, pubmed-meshheading:10476029-Blotting, Southern, pubmed-meshheading:10476029-Calcium-Binding Proteins, pubmed-meshheading:10476029-Clostridium perfringens, pubmed-meshheading:10476029-Enterotoxins, pubmed-meshheading:10476029-Female, pubmed-meshheading:10476029-Foodborne Diseases, pubmed-meshheading:10476029-Gastrointestinal Diseases, pubmed-meshheading:10476029-Gene Expression Regulation, Bacterial, pubmed-meshheading:10476029-Genetic Complementation Test, pubmed-meshheading:10476029-Humans, pubmed-meshheading:10476029-Ileum, pubmed-meshheading:10476029-Male, pubmed-meshheading:10476029-Mutation, pubmed-meshheading:10476029-Polymerase Chain Reaction, pubmed-meshheading:10476029-Rabbits, pubmed-meshheading:10476029-Species Specificity, pubmed-meshheading:10476029-Type C Phospholipases, pubmed-meshheading:10476029-Virulence
pubmed:year
1999
pubmed:articleTitle
Inactivation of the gene (cpe) encoding Clostridium perfringens enterotoxin eliminates the ability of two cpe-positive C. perfringens type A human gastrointestinal disease isolates to affect rabbit ileal loops.
pubmed:affiliation
Department of Molecular Genetics and Biochemistry, E1240 Biomedical Science Tower, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.