Secreted autotransporter toxin produced by probiotic Escherichia coli Nissle 1917 enhances neurodegeneration in Caenorhabditis elegans.

Abstract

First isolated during World War I, Escherichia coli Nissle 1917 (ECN) is an intensively studied bacterium that produces several factors that can inhibit pathogenic bacteria to promote gut health. These findings have led to its commercialization as a probiotic bacterium widely available for human consumption. Notably, the genome of ECN is highly analogous to many extraintestinal pathogenic E. coli (ExPEC) strains that do cause diseases in humans. Both ECN and ExPEC carry the sat gene which encodes a cytotoxic serine autotransporter toxin (Sat). Given that the role of ECN Sat in human disease has been poorly studied, we sought to implement the nematode C. elegans as a model for analyzing how ECN Sat may impact human neurodegenerative disease. Using multiple C. elegans disease models, we find that ECN Sat induces significantly higher neurodegeneration in several C. elegans models we tested. Although preliminary, our early findings suggest that careful studies are paramount to assess the impact of ECN to humans susceptible of neurodegenerative disease to determine the long-term safety of ECN as a commercial probiotic.