| pubmed-article:7518809 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:7518809 | lifeskim:mentions | umls-concept:C0014834 | lld:lifeskim |
| pubmed-article:7518809 | lifeskim:mentions | umls-concept:C1167622 | lld:lifeskim |
| pubmed-article:7518809 | lifeskim:mentions | umls-concept:C0449943 | lld:lifeskim |
| pubmed-article:7518809 | lifeskim:mentions | umls-concept:C0871161 | lld:lifeskim |
| pubmed-article:7518809 | pubmed:issue | 8 | lld:pubmed |
| pubmed-article:7518809 | pubmed:dateCreated | 1994-8-24 | lld:pubmed |
| pubmed-article:7518809 | pubmed:abstractText | Infection of humans with verotoxin-producing Escherichia coli (VTEC) O113:H21 is associated with clinical features comparable to those associated with infection with attaching and effacing VTEC strains including those of serotype O157:H7. We have shown previously that the adhesion phenotype of VTEC O157:H7 is influenced by the presence of a homolog of the chromosomal eaeA (for E. coli attaching and effacing) gene. In contrast, by colony blot hybridization, VTEC O113:H21 is negative for the eaeA gene. Therefore, the aim of this study was to define the adhesion phenotype of VTEC O113:H21 strain CL-15 to both cultured epithelial cells (HEp-2) and rabbit intestine in vivo. Under transmission electron microscopy, areas of microvillus effacement were observed in regions directly beneath the organism in CL-15-infected cells both in vitro and in vivo. However, F-actin adhesion pedestals on the host plasma membrane were absent. Failure of CL-15 to induce polymerization of actin was confirmed by using staining of F-actin with fluorescein-labeled phalloidin. Under indirect immunofluorescence microscopy, CL-15-infected HEp-2 cells also failed to demonstrate the recruitment of another cytoskeletal element, alpha-actinin, below foci of bacterial adhesion. In contrast, VTEC O157:H7 infection of HEp-2 cells was associated with increased alpha-actinin immunofluorescence. These findings suggest that bacterial factors distinct from those of EaeA are necessary for the adhesion phenotype of VTEC O113:H21. | lld:pubmed |
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| pubmed-article:7518809 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:7518809 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:7518809 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:7518809 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:7518809 | pubmed:issn | 0019-9567 | lld:pubmed |
| pubmed-article:7518809 | pubmed:author | pubmed-author:ShermanP MPM | lld:pubmed |
| pubmed-article:7518809 | pubmed:author | pubmed-author:BruntonJ LJL | lld:pubmed |
| pubmed-article:7518809 | pubmed:author | pubmed-author:SongPP | lld:pubmed |
| pubmed-article:7518809 | pubmed:author | pubmed-author:PhilpottD JDJ | lld:pubmed |
| pubmed-article:7518809 | pubmed:author | pubmed-author:DytocM TMT | lld:pubmed |
| pubmed-article:7518809 | pubmed:author | pubmed-author:IsmailiAA | lld:pubmed |
| pubmed-article:7518809 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:7518809 | pubmed:volume | 62 | lld:pubmed |
| pubmed-article:7518809 | pubmed:geneSymbol | eaeA | lld:pubmed |
| pubmed-article:7518809 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:7518809 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:7518809 | pubmed:pagination | 3494-505 | lld:pubmed |
| pubmed-article:7518809 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:7518809 | pubmed:year | 1994 | lld:pubmed |
| pubmed-article:7518809 | pubmed:articleTitle | Distinct binding properties of eaeA-negative verocytotoxin-producing Escherichia coli of serotype O113:H21. | lld:pubmed |
| pubmed-article:7518809 | pubmed:affiliation | Division of Gastroenterology, Hospital for Sick Children, Toronto, Ontario, Canada. | lld:pubmed |
| pubmed-article:7518809 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:7518809 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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