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Infection and Immunity, October 2006, p. 5445-5455, Vol. 74, No. 10
0019-9567/06/$08.00+0     doi:10.1128/IAI.00099-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Autoinducer 3 and Epinephrine Signaling in the Kinetics of Locus of Enterocyte Effacement Gene Expression in Enterohemorrhagic Escherichia coli

Matthew Walters and Vanessa Sperandio*

Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9048

Received 19 January 2006/ Returned for modification 7 April 2006/ Accepted 11 July 2006

Enterohemorrhagic Escherichia coli (EHEC) O157:H7 is responsible for causing outbreaks of bloody diarrhea and hemolytic-uremic syndrome throughout the world. The locus of enterocyte effacement (LEE) consists of five major operons and is required for the formation of attaching and effacing lesions that disrupt intestinal epithelial microvilli. We have previously reported that expression of EHEC LEE genes is regulated by the luxS quorum-sensing system. The luxS gene in EHEC affects the production of autoinducer 3 (AI-3), which activates the LEE. Epinephrine and norepinephrine also activate the LEE in a manner similar to that of AI-3. Previous studies of quorum-sensing regulation of LEE transcription have thus far been restricted to using reporter systems in an E. coli K-12 background. Here, we examined the kinetics of LEE gene transcription, protein expression, and function of the LEE type III secretion apparatus in wild-type (WT) EHEC and an isogenic luxS mutant. The results revealed that the luxS mutant had diminished transcription from the LEE promoters during the mid-exponential growth phase; decreased protein levels of EscJ, Tir, and EspA; and reduced secretion of EspA and EspB. The luxS mutation also caused a delay in the formation of attaching and effacing lesions on cultured epithelial cells compared to the wild type. Epinephrine enhanced LEE expression in both the WT and the luxS mutant, but the WT still exhibited greater LEE activation. The results suggest a possible synergistic relationship between AI-3 and epinephrine. The combined effects of these two signaling molecules may lead to greater LEE expression and a more efficient infection.

* 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, October 2006, p. 5445-5455, Vol. 74, No. 10
0019-9567/06/$08.00+0     doi:10.1128/IAI.00099-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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