Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1992-6-23
pubmed:abstractText
Although penetration of the epithelial mucosa has not been identified as a virulence mechanism in enterotoxigenic Escherichia coli (ETEC), we have found that this pathogen is capable of invading human intestinal cell lines. Classical ETEC strain H10407 was most invasive for epithelial cell lines derived from ileocecal and colonic tissues. An ETEC cosmid library was screened for clones that could direct E. coli HB101 to invade cultured human ileocecal epithelial cells (HCT 8 cells). Three invasive recombinant cosmid clones were isolated. These cosmids could direct HB101 invasion at an efficiency that was equal to or greater than that of the parent ETEC strain. The invasion cosmids also allowed for enhanced HCT 8 cell adherence by HB101. Electron micrographs of ETEC and recombinant HB101 strains revealed intracellular bacteria contained within endocytic vacuoles. Restriction endonuclease mapping and hybridization analyses showed that the three ETEC clones represent two separate invasion systems present in the parent ETEC strain and that both systems are chromosomally encoded. The parent ETEC strain and one cloned invasion system did not invade HeLa cells. Interestingly, one cloned invasion system was capable of directing HB101 to invade HeLa cells. Invasion of HCT 8 cells by recombinant HB101 strains and the parent ETEC strain was inhibited by cytochalasin D, indicating that the wild-type and both cloned invasion systems trigger an actin polymerization-dependent uptake process. It is not known whether the invasive phenotype of ETEC is relevant for enterotoxigenic disease. However, the parent ETEC strain, as well as recombinant HB101 strains, was capable of transcytosis through polarized HCT 8 monolayers. This transcytosis suggests that ETEC may cross the gut epithelium in vivo and that this invasion may have a previously unrecognized role in the disease process.
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/1587608-1100526, http://linkedlifedata.com/resource/pubmed/commentcorrection/1587608-1195397, http://linkedlifedata.com/resource/pubmed/commentcorrection/1587608-16562000, http://linkedlifedata.com/resource/pubmed/commentcorrection/1587608-1680136, http://linkedlifedata.com/resource/pubmed/commentcorrection/1587608-1682258, http://linkedlifedata.com/resource/pubmed/commentcorrection/1587608-1688838, http://linkedlifedata.com/resource/pubmed/commentcorrection/1587608-1879916, http://linkedlifedata.com/resource/pubmed/commentcorrection/1587608-1937792, http://linkedlifedata.com/resource/pubmed/commentcorrection/1587608-2052421, http://linkedlifedata.com/resource/pubmed/commentcorrection/1587608-2172966, http://linkedlifedata.com/resource/pubmed/commentcorrection/1587608-2180823, http://linkedlifedata.com/resource/pubmed/commentcorrection/1587608-2182543, http://linkedlifedata.com/resource/pubmed/commentcorrection/1587608-2311122, http://linkedlifedata.com/resource/pubmed/commentcorrection/1587608-2459066, http://linkedlifedata.com/resource/pubmed/commentcorrection/1587608-2548211, http://linkedlifedata.com/resource/pubmed/commentcorrection/1587608-2642465, http://linkedlifedata.com/resource/pubmed/commentcorrection/1587608-2662196, http://linkedlifedata.com/resource/pubmed/commentcorrection/1587608-2668429, http://linkedlifedata.com/resource/pubmed/commentcorrection/1587608-2826335, http://linkedlifedata.com/resource/pubmed/commentcorrection/1587608-2830310, http://linkedlifedata.com/resource/pubmed/commentcorrection/1587608-2833444, http://linkedlifedata.com/resource/pubmed/commentcorrection/1587608-2989179, http://linkedlifedata.com/resource/pubmed/commentcorrection/1587608-327080, http://linkedlifedata.com/resource/pubmed/commentcorrection/1587608-3294797, http://linkedlifedata.com/resource/pubmed/commentcorrection/1587608-3304658, http://linkedlifedata.com/resource/pubmed/commentcorrection/1587608-351079, http://linkedlifedata.com/resource/pubmed/commentcorrection/1587608-3543152, http://linkedlifedata.com/resource/pubmed/commentcorrection/1587608-3891253, http://linkedlifedata.com/resource/pubmed/commentcorrection/1587608-4826581, http://linkedlifedata.com/resource/pubmed/commentcorrection/1587608-4863722, http://linkedlifedata.com/resource/pubmed/commentcorrection/1587608-4896022, http://linkedlifedata.com/resource/pubmed/commentcorrection/1587608-4926260, http://linkedlifedata.com/resource/pubmed/commentcorrection/1587608-4926261, http://linkedlifedata.com/resource/pubmed/commentcorrection/1587608-4996788, http://linkedlifedata.com/resource/pubmed/commentcorrection/1587608-6260575, http://linkedlifedata.com/resource/pubmed/commentcorrection/1587608-6350186, http://linkedlifedata.com/resource/pubmed/commentcorrection/1587608-6352891, http://linkedlifedata.com/resource/pubmed/commentcorrection/1587608-785259
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0019-9567
pubmed:author
pubmed:issnType
Print
pubmed:volume
60
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2409-17
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1992
pubmed:articleTitle
Molecular cloning of epithelial cell invasion determinants from enterotoxigenic Escherichia coli.
pubmed:affiliation
Department of Bacterial Immunology, Walter Reed Army Institute of Research, Washington, D.C. 20307-5100.
pubmed:publicationType
Journal Article