E. coli infections could be reduced with probiotics, show non-human studies
There is no cure for E. coli infections such as those that adhere to epithelial cells in the gut (enterohemorrhagic E. coli - or EHEC), but probiotic supplier Winclove Bio Industries is highlighting existing non-human research that explores probiotic potential in the area.
While the Dutch supplier acknowledges the data so far collected is purely in vitro, such results bear closer scrutiny given ‘the E. coli crisis’ that saw about 50 people die, and was followed by the European Union stumping up €210m to boost the hard-hit fruit and vegetable sector in the wake of the crisis.
Typical symptoms of the problem are abdominal cramps and watery or bloody diarrhoea which can lead to hemolytic-uremic syndrome (HUS), which can shut down the kidneys. It is most common in children and the elderly.
While the recent infections were caused by the E. coli strain 0104:H4, whereas most of the in vitro work has been performed another E. coli variant: 0157:H7. But the encouraging anti-adhesion results there gave merit to exploring probiotic effects for 0104:H4.
“In vitro studies have shown that probiotics may be effective in controlling infections caused by E. coli 0157:H7 on all three levels,” Winclove said. Those levels are microbial interaction; epithelium interaction and immune system interaction.
Bifidobacteria and Lactibacillus strains had shown the most potential.
For example, L. acidophilus had been shown to positively effect the upregulation of intestinal tract mucins and the subsequent inhibition of attachment of E. coli 0157:H.
Winclove said: “The discussed results have not been obtained from experiments in humans, however it is reasonable to assume that at least some of these results can be extrapolated. Therefore, it is worthwhile investigating the probiotic capabilities to control the [toxin] production and disease symptoms caused by E. coli 0104:H4 in human gut cells.”
Rather than invading gut mucosa, EHEC can induce cytoskeletal rearrangements in infected epithelial cells leading to lesions that alter intestinal permeability.
HUS is thought to be caused by the Shiga toxins that are transported through the bloodstream by neutrophils binding to target cell surface receptors resulting into cell apoptosis, Winclove observed.
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