| Autor: |
Lloyd, Sonja J., Ritchie, Jennifer M., Rojas-Lopez, Maricarmen, Blumentritt, Carla A., Popov, Vsevolod L., Greenwich, Jennifer L., Waldor, Matthew K., Torres, Alfredo G. |
| Zdroj: |
Infection and Immunity; March 2012, Vol. 80 Issue: 3 p914-920, 7p |
| Abstrakt: |
Escherichia coliO157:H7 causes food and waterborne enteric infections that can result in hemorrhagic colitis and life-threatening hemolytic uremic syndrome. Intimate adherence of the bacteria to intestinal epithelial cells is mediated by intimin, but E. coliO157:H7 also possess several other putative adhesins, including curli and two operons that encode long polar fimbriae (Lpf). To assess the importance of Lpf for intestinal colonization, we performed competition experiments between E. coliO157:H7 and an isogenic ?lpfA1?lpfA2double mutant in the infant rabbit model. The mutant was outcompeted in the ileum, cecum, and midcolon, suggesting that Lpf contributes to intestinal colonization. In contrast, the ?lpfA1?lpfA2mutant showed increased adherence to colonic epithelial cells in vitro. Transmission electron microscopy revealed curli-like structures on the surface of the ?lpfA1?lpfA2mutant, and the presence of curli was confirmed by Congo red binding, immunogold-labeling electron microscopy, immunoblotting, and quantitative real-time reverse transcription-PCR (qRT-PCR) measuring csgAexpression. However, deletion of csgA, which encodes the major curli subunit, does not appear to affect intestinal colonization. In addition to suggesting that Lpf can contribute to EHEC intestinal colonization, our observations indicate that the regulatory pathways governing the expression of Lpf and curli are interdependent. |
| Databáze: |
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