Initial binding of Shiga toxin-producing Escherichia coli to host cells and subsequent induction of actin rearrangements depend on filamentous EspA-containing surface appendages
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作者:
Ebel, F
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Univ Giessen, Inst Med Mikrobiol, D-35392 Giessen, GermanyUniv Giessen, Inst Med Mikrobiol, D-35392 Giessen, Germany
Ebel, F
[1
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Podzadel, T
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机构:Univ Giessen, Inst Med Mikrobiol, D-35392 Giessen, Germany
Podzadel, T
Rohde, M
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机构:Univ Giessen, Inst Med Mikrobiol, D-35392 Giessen, Germany
Rohde, M
Kresse, AU
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机构:Univ Giessen, Inst Med Mikrobiol, D-35392 Giessen, Germany
Kresse, AU
Krämer, S
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机构:Univ Giessen, Inst Med Mikrobiol, D-35392 Giessen, Germany
Krämer, S
Deibel, C
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机构:Univ Giessen, Inst Med Mikrobiol, D-35392 Giessen, Germany
Deibel, C
Guzmán, CA
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机构:Univ Giessen, Inst Med Mikrobiol, D-35392 Giessen, Germany
Guzmán, CA
Chakraborty, T
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机构:Univ Giessen, Inst Med Mikrobiol, D-35392 Giessen, Germany
Chakraborty, T
机构:
[1] Univ Giessen, Inst Med Mikrobiol, D-35392 Giessen, Germany
[2] GBF Natl Res Ctr Biotechnol, Div Microbiol, D-38124 Braunschweig, Germany
Shiga toxin-producing Escherichia coli (STEC) induce so-called attaching and effacing lesions that enable the tight adherence of these pathogens to the gut epithelium. All of the genes necessary for this process are present in the locus of enterocyte effacement, which encodes a type III secretion system, the secreted Esp proteins and the surface protein intimin. In this study we sequenced the espA gene of STEC, generated and characterized a corresponding deletion mutant and raised EspA-specific monoclonal antibodies to analyse the functional role of this protein during infection. EspA was detected in often filament-like structures decorating all bacteria that had attached to Hela cells. These appendages were especially prominent on bacteria that had not yet induced the formation of actin pedestals, indicating that they mediate the initial contact of STEC to their target cells. Consistently, a deletion of the espA gene completely abolished the capacity of such STEC mutants to bind to HeLa cells and to induce actin rearrangements. Surface appendages similar to those described in this study are also formed by Pseudomonas syringae and may represent a structural element common to many bacterial pathogens that deliver proteins into their target cells via a type ill secretion system.
机构:
STANFORD UNIV, BECKMAN CTR B239, HOWARD HUGHES MED INST, DEPT MICROBIOL & IMMUNOL, STANFORD, CA 94305 USASTANFORD UNIV, BECKMAN CTR B239, HOWARD HUGHES MED INST, DEPT MICROBIOL & IMMUNOL, STANFORD, CA 94305 USA
GIRON, JA
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HO, ASY
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STANFORD UNIV, BECKMAN CTR B239, HOWARD HUGHES MED INST, DEPT MICROBIOL & IMMUNOL, STANFORD, CA 94305 USASTANFORD UNIV, BECKMAN CTR B239, HOWARD HUGHES MED INST, DEPT MICROBIOL & IMMUNOL, STANFORD, CA 94305 USA
HO, ASY
;
SCHOOLNIK, GK
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机构:
STANFORD UNIV, BECKMAN CTR B239, HOWARD HUGHES MED INST, DEPT MICROBIOL & IMMUNOL, STANFORD, CA 94305 USASTANFORD UNIV, BECKMAN CTR B239, HOWARD HUGHES MED INST, DEPT MICROBIOL & IMMUNOL, STANFORD, CA 94305 USA
机构:
STANFORD UNIV, BECKMAN CTR B239, HOWARD HUGHES MED INST, DEPT MICROBIOL & IMMUNOL, STANFORD, CA 94305 USASTANFORD UNIV, BECKMAN CTR B239, HOWARD HUGHES MED INST, DEPT MICROBIOL & IMMUNOL, STANFORD, CA 94305 USA
GIRON, JA
;
HO, ASY
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机构:
STANFORD UNIV, BECKMAN CTR B239, HOWARD HUGHES MED INST, DEPT MICROBIOL & IMMUNOL, STANFORD, CA 94305 USASTANFORD UNIV, BECKMAN CTR B239, HOWARD HUGHES MED INST, DEPT MICROBIOL & IMMUNOL, STANFORD, CA 94305 USA
HO, ASY
;
SCHOOLNIK, GK
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机构:
STANFORD UNIV, BECKMAN CTR B239, HOWARD HUGHES MED INST, DEPT MICROBIOL & IMMUNOL, STANFORD, CA 94305 USASTANFORD UNIV, BECKMAN CTR B239, HOWARD HUGHES MED INST, DEPT MICROBIOL & IMMUNOL, STANFORD, CA 94305 USA