Some Shiga toxin-producing Escherichia coli (STEC) strains, enterohemorrhagic E. coli strains, are food-borne pathogens which evoke life-threatening diseases in humans (26). Cattle and other ruminants can shed STEC for long periods and are a major reservoir for zoonotic STEC (6,61,70,72). Emerging human STEC infections make the reduction of STEC shedding by reservoir species a current challenge in veterinary public health.Several lines of evidence indicate that STEC adherence to bovine intestinal epithelial cells is essential for long-term STEC colonization of ruminants. Within hours after oral infection, STEC O157:H7 can be detected throughout the gastrointestinal tract, including the rumen, of cattle (6, 18). As early as 4 days after inoculation, STEC strains colonize epithelial cells in the ileum, cecum, colon, rectum, and gall bladder in weaned calves (8, 59, 62). STEC O157:H7 strains principally colonize the rectoanal junction of weaned calves and older cattle (10, 33, 44), but O157:H7 colonization also can occur at other sites of the bovine intestinal tract (8,23,55). The ability of the majority of bovine STEC isolates to intimately attach to cells and rearrange the actin cytoskeleton (attachingand-effacing [AE] lesions) (71) may facilitate adherence to the intestinal epithelium (5, 9, 44). Signature-tagged mutagenesis studies showed that factors not involved in AE lesion formation further support STEC colonization of the bovine intestinal epithelium (11,68). The duration of STEC shedding correlates with epithelial cell turnover in the bovine intestine (35). Vaccination strategies directed against proteins involved in STEC adherence to the bovine intestinal mucosa have been successful in reducing STEC O157:H7 infection in cattle (49,50,52,67).Other STEC factors also may influence the duration of colonization. Recent studies suggest that STEC suppresses the bovine host's immune response, limits mucosal inflammation, and maintains intestinal homeostasis. Lymphostatin (2) and Shiga toxin 1 (Stx1) (39) block the proliferation of bovine lymphocytes in vitro. Stx1 alters the cytokine response of bovine intraepithelial lymphocytes (42), cells that are scattered within the epithelial layer and are affected in vivo by Stx1 from STEC strains that do not colonize next to organized lymphoid tissues (38). Some STEC O157:H7 strains exhibit a tropism for the follicle-associated epithelium of Peyer's patches in the bovine intestine (51) and may release modulating factors adjacent to induction sites of the immune response. Development of a cellular immune response against STEC antigens is significantly delayed in calves inoculated with Stx2-producing E. coli O157:H7 compared to that of calves inoculated with a nontoxigenic O157:H7 strain (22). Immune-modulating STEC factors are potential targets for future strategies aimed at reducing STEC shedding in cattle, but their mode of action in the bovine intestine is only partially understood.Stx proteins are potent 1A:5B-structured cytotoxins with RNA N-glycosidase activity tha...
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