Inhibition of water absorption and selective damage to human colonic mucosa are induced by subtilase cytotoxin produced by Escherichia coli O113:H21.

Abstract

Shiga toxin-producing Escherichia coli O157:H7 (STEC) is by far the most prevalent serotype associated with hemolytic uremic syndrome (HUS) although many non-O157 STEC strains have been also isolated from patients with HUS. The main virulence factor of STEC is the Shiga toxin type 2 (Stx2) present in O157 and non-O157 strains. Recently, another toxin, named subtilase cytotoxin (SubAB), has been isolated from several non-O157 strains and may contribute to the pathogenesis of HUS. Here, we have demonstrated that an O113:H21 STEC strain expressing SubAB and Stx2 inhibits normal water absorption across human colon and causes damage to the surface epithelium, necrosis, mononuclear inflammatory infiltration, edema, and marked mucin depletion. This damage was less marked, but nevertheless significant, when purified SubAB or E. coli O113:H21 expressing only SubAB was assayed. This is the first study showing that SubAB may directly participate in the mechanisms of diarrhea in children infected with non-O157 STEC strains.

• Authors: Elizabeth Gerhardt, Mariana Masso, Adrienne W Paton, James C Paton, Elsa Zotta, Cristina Ibarra
• Journal: Infection and immunity (Infect Immun) Vol. 81 Issue 8 Pg. 2931-7 (Aug 2013) ISSN: 1098-5522 [Electronic] United States
• PMID: 23732168 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Escherichia coli Proteins
• Water
• Subtilisins
• subtilase cytotoxin, E coli

Topics

• Animals
• Chlorocebus aethiops
• Colon (metabolism, pathology)
• Diarrhea (metabolism, microbiology)
• Escherichia coli Infections (complications, metabolism)
• Escherichia coli Proteins (metabolism)
• Hemolytic-Uremic Syndrome (metabolism, microbiology)
• Humans
• Intestinal Absorption (physiology)
• Intestinal Mucosa (metabolism, pathology)
• Organ Culture Techniques
• Shiga-Toxigenic Escherichia coli (metabolism, pathogenicity)
• Subtilisins (metabolism)
• Vero Cells
• Water