Journal of Antimicrobial Chemotherapy, Vol 42, 341-347, Copyright © 1998 by The British Society for Antimicrobial Chemotherapy
K Izumikawa, Y Hirakata, T Yamaguchi, H Takemura, S Maesaki, K Tomono, S Igimi, M Kaku, Y Yamada, S Kohno and S Kamihira
It is not clear how Escherichia coli O157 invades human enteric epithelium
and causes the haemolytic uraemic syndrome (HUS), and nor has the most
appropriate treatment of E. coli O157 infection been established.
Verotoxins, leucocytes and proinflammatory cytokines, such as tumour
necrosis factor-alpha (TNF-alpha), interleukin (IL)-6 and IL- 8, are
considered essential for the development of HUS. We used the Caco-2 cell
monolayer system, well-known as an in-vitro model of human intestinal
infection, to determine how E. coli O157 interacts with intestinal
epithelial cells and also studied the influence of fosfomycin on the
virulence of the bacteria. Results showed that the E. coli O157 used in
this study did not penetrate the Caco-2 cell monolayer system, unlike
Salmonella typhimurium SL1344, and verotoxin 1 (VT 1), but not VT 2,
translocated across the system. In an in-vitro conventional assay,
fosfomycin increased the amount of verotoxins but it did not influence
penetration of bacteria and translocation of verotoxins in the Caco-2 cell
monolayer system. The production of both IL-8 (a potent neutrophil
activator) and TNF-alpha in the human monocytic THP-1 cell line was reduced
by fosfomycin-treated basolateral medium in this system. These results
indicate that fosfomycin may be a potent drug for preventing HUS caused by
E. coli O157 infection.
ORIGINAL ARTICLES
Escherichia coli O157 interactions with human intestinal Caco-2 cells and the influence of fosfomycin
Department of Laboratory Medicine, Nagasaki University School of Medicine, Sakamoto, Japan.
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