pubmed-article:15727837 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:15727837 | lifeskim:mentions | umls-concept:C0014834 | lld:lifeskim |
pubmed-article:15727837 | lifeskim:mentions | umls-concept:C0021853 | lld:lifeskim |
pubmed-article:15727837 | lifeskim:mentions | umls-concept:C1158770 | lld:lifeskim |
pubmed-article:15727837 | lifeskim:mentions | umls-concept:C1880177 | lld:lifeskim |
pubmed-article:15727837 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:15727837 | pubmed:dateCreated | 2005-2-24 | lld:pubmed |
pubmed-article:15727837 | pubmed:abstractText | The Escherichia coli regulatory protein RfaH contributes to efficient colonization of the mouse gut. Extraintestinal pathogenic (ExPEC) as well as non-pathogenic probiotic E. coli strains rapidly outcompeted their isogenic rfaH mutants following oral mixed infections. LPS-core and O-antigen side-chain as well as capsular polysaccharide synthesis are among the E. coli virulence factors affected by RfaH. In respect of colonization, deep-rough LPS mutants (waaG) but not capsular (kps) mutants were shown to behave similarly to rfaH mutants. Furthermore, alteration in the length of O-antigen side-chains did not modify colonization ability either indicating that it was the regulatory effect of RfaH on LPS-core synthesis, which affected intestinal colonization. Loss of RfaH did not significantly influence adhesion of bacteria to cultured colon epithelial cells. Increased susceptibility of rfaH mutants to bile salts, on the other hand, suggested that impaired in vivo survival could be responsible for the reduced colonization capacity. | lld:pubmed |
pubmed-article:15727837 | pubmed:language | eng | lld:pubmed |
pubmed-article:15727837 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15727837 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:15727837 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:15727837 | pubmed:month | Mar | lld:pubmed |
pubmed-article:15727837 | pubmed:issn | 0378-1097 | lld:pubmed |
pubmed-article:15727837 | pubmed:author | pubmed-author:DobrindtUlric... | lld:pubmed |
pubmed-article:15727837 | pubmed:author | pubmed-author:HackerJörgJ | lld:pubmed |
pubmed-article:15727837 | pubmed:author | pubmed-author:NagyGáborG | lld:pubmed |
pubmed-article:15727837 | pubmed:author | pubmed-author:GrozdanovLubo... | lld:pubmed |
pubmed-article:15727837 | pubmed:author | pubmed-author:EmodyLeventeL | lld:pubmed |
pubmed-article:15727837 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:15727837 | pubmed:day | 1 | lld:pubmed |
pubmed-article:15727837 | pubmed:volume | 244 | lld:pubmed |
pubmed-article:15727837 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:15727837 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:15727837 | pubmed:pagination | 173-80 | lld:pubmed |
pubmed-article:15727837 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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pubmed-article:15727837 | pubmed:year | 2005 | lld:pubmed |
pubmed-article:15727837 | pubmed:articleTitle | Transcriptional regulation through RfaH contributes to intestinal colonization by Escherichia coli. | lld:pubmed |
pubmed-article:15727837 | pubmed:affiliation | Department of Medical Microbiology and Immunology, University of Pécs, 7624 Pécs Szigeti út 12, Hungary. gabor.nagy@aok.pte.hu | lld:pubmed |
pubmed-article:15727837 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:15727837 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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