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| Research article summary (published 12 Nov 2009): |
Synergistic role of curli and cellulose in cell adherence and biofilm formation of attaching and effacing Escherichia coli and identification of Fis as a negative regulator of curli.
Full Abstract
Curli are adhesive fimbriae of Escherichia coli and Salmonella enterica. Expression of curli (csgA) and cellulose (bcsA) is co-activated by the transcriptional activator CsgD. In this study, we investigated the contribution of curli and cellulose to the adhesive properties of enterohaemorragic (EHEC) O157:H7 and enteropathogenic E. coli (EPEC) O127:H6. While single mutations in csgA, csgD or bcsA in EPEC and EHEC had no dramatic effect on cell adherence, double csgAbcsA mutants were significantly less adherent than the single mutants or wild-type strains to human colonic HT-29 epithelial cells or to cow colon tissue in vitro. Overexpression of csgD (carried on plasmid pCP994) in a csgD mutant, but not in the single csgA or bscA mutants, led to significant increase in adherence and biofilm formation in EPEC and EHEC, suggesting that synchronized over-production of curli and cellulose enhances bacterial adherence. In line with this finding, csgD transcription was activated significantly in the presence of cultured epithelial cells as compared with growth in tissue culture medium. Analysis of the influence of virulence and global regulators in the production of curli in EPEC identified Fis (factor for inversion stimulation) as a, heretofore unrecognized, negative transcriptional regulator of csgA expression. An EPEC E2348/69Deltafis produced abundant amounts of curli whereas a double fis/csgD mutant yielded no detectable curli production. Our data suggest that curli and cellulose act in concert to favour host colonization, biofilm formation and survival in different environments.
Author information
Author/s: Saldaña, Zeus (Z); Xicohtencatl-Cortes, Juan (J); Avelino, Fabiola (F); Phillips, Alan D (AD); Kaper, James B (JB); Puente, José L (JL); Girón, Jorge A (JA);
Affiliation: Department of Immunobiology, University of Arizona, 1501 N. Tucson, AZ 85724, USA.
Grants: AI063211 (Agency:NIAID NIH HHS) ; AI066012 (Agency:NIAID NIH HHS) ; AI21657 (Agency:NIAID NIH HHS)
Journal and publication information
Publication Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
Journal: Environmental microbiology (Environ Microbiol), published in England. (Language: eng)
Reference: 2009-Apr; vol 11 (issue 4) : pp 992-1006
Dates: Created 2009/04/23; Completed 2009/05/22;
PMID: 19187284, status: MEDLINE (last retrieval date: 5/22/2009, IMS Date: )
Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.
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