Inhibition of water absorption and selective damage to human colonic mucosa induced by Shiga toxin-2 are enhanced by Escherichia coli O157:H7 infection

ALBANESE ADRIANA; GERHARD ELIZABETH; GARCÍA HUGO; AMIGO NATALIA; CATALDI ANGEL; ZOTTA ELSA; IBARRA CRISTINA

INTERNATIONAL JOURNAL OF MEDICAL MICROBIOLOGY (PRINT)

ELSEVIER GMBH

Año: 2015 vol. 305 p. 348 - 354

1438-4221

tShiga toxin-producing Escherichia coli (STEC) strains are responsible for a variety of clinical syndromesincluding bloody and non-bloody diarrhea, hemorrhagic colitis, and hemolytic uremic syndrome (HUS).Although multiple serotypes of STEC have been isolated from hemorrhagic colitis cases, E. coli O157:H7 isby far the most prevalent serotype associated with HUS. Shiga toxin is the major virulence factor of E. coliO157:H7 and is responsible for the more severe symptoms of the infection. However, the mechanismsinvolved in the pathogenesis of diarrhea mediated by Stx2 are not well known. In this study, we havedetermined the effects of E. coli O157:H7 strain 125/99 wild type (wt) on the human colonic mucosamounted in an Ussing chamber. In response to 125/99wt, an inhibition of water absorption across humancolonic mucosa was observed. Histological sections showed severe necrosis with detachment of thesurface epithelium, mononuclear inflammatory infiltrate and loss of goblet cells after 1 h of incubationwith 125/99wt. These alterations were not observed with the isogenic mutant strain lacking stx2 or withthe filter-sterilized culture supernatant from the 125/99wt strain. These results indicate that the celldamages in human colon are induced by Stx2, and that Stx2 production is increased by the interactionwith bacterial cells. Identification of host cell-derived factors responsible for increasing Stx2 can lead tonew strategies for modulating STEC infections.