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Infection and Immunity, December 1999, p. 6670-6677, Vol. 67, No. 12
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Shiga Toxins 1 and 2 Translocate Differently across Polarized Intestinal Epithelial Cells

Bryan P. Hurley,1 Mary Jacewicz,1 C. M. Thorpe,1 Lisa L. Lincicome,1 Andrew J. King,2 Gerald T. Keusch,1,dagger and David W. K. Acheson1,*

Division of Geographic Medicine and Infectious Disease1 and Division of Nephrology,2 New England Medical Center, Boston, Massachusetts 02111

Received 27 May 1999/Returned for modification 14 July 1999/Accepted 17 September 1999

Shiga toxin-producing Escherichia coli (STEC) is an important food-borne pathogen that causes hemolytic-uremic syndrome. Following ingestion, STEC cells colonize the intestine and produce Shiga toxins (Stx), which appear to translocate across the intestinal epithelium and subsequently reach sensitive endothelial cell beds. STEC cells produce one or both of two major toxins, Stx1 and Stx2. Stx2-producing STEC is more often associated with disease for reasons as yet undetermined. In this study, we used polarized intestinal epithelial cells grown on permeable filters as a model to compare Stx1 and Stx2 movement across the intestinal epithelium. We have previously shown that biologically active Stx1 is able to translocate across cell monolayers in an energy-dependent, saturable manner. This study demonstrates that biologically active Stx2 is also capable of movement across the epithelium without affecting barrier function, but significantly less Stx2 crossed monolayers than Stx1. Chilling the monolayers to 4°C reduced the amount of Stx1 and Stx2 movement by 200-fold and 20-fold respectively. Stx1 movement was clearly directional, favoring an apical-to-basolateral translocation, whereas Stx2 movement was not. Colchicine reduced Stx1, but not Stx2, translocation. Monensin reduced the translocation of both toxins, but the effect was more pronounced with Stx1. Brefeldin A had no effect on either toxin. Excess unlabeled Stx1 blocks the movement of 125I-Stx1. Excess Stx2 failed to have any effect on Stx1 movement. Our data suggests that, despite the many common physical and biochemical properties of the two toxins, they appear to be crossing the epithelial cell barrier by different pathways.

* Corresponding author. Mailing address: Division of Geographic Medicine and Infectious Diseases, New England Medical Center, Box 041, 750 Washington St., Boston, MA 02111. Phone: (617) 636-7002. Fax: (617) 636-5292. E-mail: david.acheson{at}es.nemc.org.

dagger Present address: Fogarty International Center, National Institutes of Health, Bethesda, MD.

Infection and Immunity, December 1999, p. 6670-6677, Vol. 67, No. 12
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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