Shiga toxin-producing Escherichia coli can impair T84 cell structure and function without inducing attaching/effacing lesions

Enteropathogenic Escherichia coli (EPEC) intimately adhere to epithelial ce lls producing cytoskeletal rearrangement with typical attaching and effacin g lesions and altered epithelial barrier and transport function. Since EPEC and Shiga toxin-producing E. coli (STEC) share similar genes in the "locus for enterocyte effacement" (LEE) thought to cause these changes, it has be en assumed that STEC shares similar pathogenic mechanisms with EPEC. The ai ms of this study were to compare the effects of EPEC and STEC on bacterial- epithelial interactions and to examine changes in epithelial function. T84 monolayers were infected with STEC O157:H7 (wild strain EDL 933 or non-toxi n-producing strain 85/170), EPEC (strain E2348/69), or HB101 (nonpathogenic ) and studied at various times after infection. EPEC bound more avidly than EDL 933, but both strains exhibited greater binding than HB101. Attaching and effacing lesions and severe disruption to the actin cytoskeleton were o bserved in EPEC by 3 h postinfection but not in EDL 933 or HB101 at any tim e point, EPEC and EDL 933 increased monolayer permeability to [H-3]mannitol 5- to 10-fold. In contrast to EPEC, EDL 933 completely abolished secretago gue-stimulated anion secretion as assessed under voltage clamp conditions i n Ussing chambers. Several other STEC strains induced changes similar to th ose of EDL 933. In conclusion, STEC impairs epithelial barrier function and ion transport without causing major disruption to the actin cytoskeleton, Pathogenic factors other than products of LEE may be operant in STEC.