Submitted to: Foodborne Pathogens and Disease
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/3/2012
Publication Date: 3/19/2013
Citation: Kudva, I.T., Hovde, C.J., John, M. 2013. Adherence of non-O157 Shiga-toxin Escherichia coli to bovine recto-anal junction squamous epithelial cells appears to be mediated by mechanisms distinct from those used by O157. Foodborne Pathogens and Disease. 10(4):375-381. Interpretive Summary: Shiga-toxin producing Eshcerichia coli (STEC) are a major source of foodborne infections in the United States, causing about 113,000 illnesses and 300 hospitalizations. The illness starting with diarrhea can either stop at this symptom or progress to serious consequences that can affect major organs of the body with fatal outcomes. Ruminant animals (cattle, sheep) carry these STECs in their intestines, without developing disease, and act as the major food source transmitting these STECs to humans. In order to develop measures to eliminate STECs from ruminant animal intestines we need to understand the mechanisms used by STECs to attach and survive in the same. We recently developed an assay using cattle intestine cells to study attachment of one STEC, O157, in the laboratory without using the whole animal. In this study, we have successfully used this assay to study the interactions of other STECs declared as food adultrants, O26, O103, O111, O121, O145 and O45, with cattle intestine cells. Our results show that all these six STECs adhere to this set of cattle intestine cells using hitherto uncharacterized proteins, and these may be different from the proteins used by O157. This finding is important (1) if we are to develop effective vaccines/therapies that would prevent STEC attachment to cattle intestines and (2) when designing cross-protective vaccines.
Technical Abstract: This study presents evidence that the pattern of adherence of clinically relevant non-O157 Shiga-toxin producing Escherichia coli (STEC) to bovine recto-anal junction squamous epithelial cells (RSE) is similar to that of O157, although the mechanisms of adherence appear to be distinct. Our results further suggest that novel adhesins, and not Intimin, are likely involved in non-O157 STEC adherence to bovine RSE cells. These findings have important implications for the development of efficacious modalities for blocking adherence of these STECs to bovine gastrointestinal epithelial cells.