Linked Life Data

8900070

Source:http://linkedlifedata.com/resource/pubmed/id/8900070

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2-3
pubmed:dateCreated
1997-2-5
pubmed:databankReference
pubmed:abstractText
A number of enteric pathogens, including enteropathogenic (EPEC) and enterohemorrhagic (EHEC) Escherichia coli, Hafnia alvei, a strain of Citrobacter freundii, and rabbit EPEC strain RDEC-1 cause attaching-effacing (AE) lesions in the gut mucosa. These bacteria have a pathogenicity cassette (locus of enterocyte effacement or LEE) containing the eaeA gene. This gene encodes intimin, an outer membrane protein required for production of AE lesions. RDEC-1, a non-invasive enteropathogen in young rabbits, produces AE lesions morphologically indistinguishable from lesions caused by human AE bacterial strains. The RDEC-1 example of E. coli diarrhea in rabbits is an important model for studying the pathogenesis of AE bacteria in a natural infection and for analyzing specific roles of the components of LEE. In order to better understand the role of intimin in the development of AE lesions, a portion of DNA within RDEC-1 LEE, containing the eaeA gene and an upstream open reading frame (ORF), was sequenced. The RDEC-1 eaeA gene shared 87%, 92%, and 93% DNA sequence identity and > 80% amino acid sequence identity with the eaeA genes of C. freundii biotype 4280, EHEC O157:H7, and EPEC O127:116, respectively. The carboxy-terminal 280 amino acid residues of intimin has 80%, 56%, and 54% identity with C. freundii, EHEC O157:H7, and EPEC O127:H6 intimins, respectively. The predicted protein encoded by the upstream ORF (156 amino acids) shares 95%, 97%, and 99% amino acid identity with predicted proteins from C. freundii. EHEC O157:H7, and EPEC O127:H6, respectively. The high degree of sequence homology of the ORF and the eueA gene of RDEC-1 with those of other AE bacteria suggests an evolutionary relationship of LEE and supports and facilitates the use of the RDEC-1 model for studying the role of LEE in pathogenesis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0378-1097
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
144
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
249-58
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:8900070-Adhesins, Bacterial, pubmed-meshheading:8900070-Amino Acid Sequence, pubmed-meshheading:8900070-Animals, pubmed-meshheading:8900070-Bacterial Outer Membrane Proteins, pubmed-meshheading:8900070-Base Sequence, pubmed-meshheading:8900070-Carrier Proteins, pubmed-meshheading:8900070-Diarrhea, pubmed-meshheading:8900070-Disease Models, Animal, pubmed-meshheading:8900070-Escherichia coli, pubmed-meshheading:8900070-Escherichia coli Infections, pubmed-meshheading:8900070-Escherichia coli Proteins, pubmed-meshheading:8900070-Evolution, Molecular, pubmed-meshheading:8900070-Genes, Bacterial, pubmed-meshheading:8900070-Humans, pubmed-meshheading:8900070-Molecular Sequence Data, pubmed-meshheading:8900070-Open Reading Frames, pubmed-meshheading:8900070-Rabbits, pubmed-meshheading:8900070-Species Specificity
pubmed:year
1996
pubmed:articleTitle
Characterization of the eaeA gene from rabbit enteropathogenic Escherichia coli strain RDEC-1 and comparison to other eaeA genes from bacteria that cause attaching-effacing lesions.
pubmed:affiliation
Walter Reed Army Institute of Research, Washington, DC 20307-5100, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't