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Infection and Immunity, April 2004, p. 2329-2337, Vol. 72, No. 4
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.4.2329-2337.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Modulation of Enteropathogenic Escherichia coli Virulence by Quorum Sensing

Marcelo P. Sircili,1,2 Matthew Walters,1 Luis R. Trabulsi,2 and Vanessa Sperandio1*

Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, Texas,1 Laboratorio Especial de Microbiologia, Instituto Butanta, Sao Paulo, Brazil2

Received 6 October 2003/ Returned for modification 19 December 2003/ Accepted 27 December 2003

Enteropathogenic Escherichia coli (EPEC) produces a lesion on epithelial cells called the attaching and effacing (AE) lesion. All genes necessary for AE are encoded within the locus of enterocyte effacement (LEE). EPEC also adheres in a characteristic pattern to epithelial cells by forming microcolonies, usually referred to as localized adherence (LA). LA is mediated by the bundle-forming pilus and flagella. The LEE genes are directly activated by the LEE-encoded regulator (Ler). Transcription of Ler is under the control of Per, integration host factor, Fis, BipA, and quorum sensing (QS), specifically through the luxS system. QS activates expression of the LEE genes in EPEC, with QseA activating transcription of ler. Here we report that transcription of the LEE genes and type III secretion are diminished in both luxS and qseA mutants. Transcription of the LEE genes is affected in both mutants mostly during the mid-exponential phase of growth. Transcription of qseA itself is diminished throughout growth in a luxS mutant and is under autorepression. Furthermore, QS activation of type III secretion is independent of per, given that QseA still activates type III secretion in a per mutant strain. Both mutants are deficient in adherence to epithelial cells and form smaller microcolonies. Several factors may contribute to this abnormal behavior: transcription of LEE genes and type III secretion are diminished, and expression of flagella and Per is altered in both mutants. These results suggest that QS is involved in modulating the regulation of the EPEC virulence genes.

* Corresponding author. Mailing address: University of Texas Southwestern Medical Center, Dept. of Microbiology, 5323 Harry Hines Blvd., Dallas, TX 75390-9048. Phone: (214) 648-1603. Fax: (214) 648-5905. E-mail: vanessa.sperandio{at}utsouthwestern.edu.

Editor: V. J. DiRita

Infection and Immunity, April 2004, p. 2329-2337, Vol. 72, No. 4
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.4.2329-2337.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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