Recombinant shiga toxin 1 subunit b [His]

Safety in raw milk cheeses being a major public health issue, the aim of this study was to validate a new bio preservation strategy by evaluating the efficacy of an inhibitory bacterial consortium (Hafnia alvei, Lactobacillus plantarum and Lactococcus lactis) on the growth of E. coli O26:H11 in uncooked pressed cheeses manufactured with different raw milk batches (6 farms, 3 periods). The pathogen was inoculated at very low concentrations (0.5 and 0.05 cfu mL(-1)), close to reality. The inhibitory power of the consortium was determined by culture analyses, and 16S rDNA sequencing of milk batches and cheeses was performed to evaluate the impact of milk microbial composition on the consortium's inhibition capacities. Raw milk batches differed in their fat and protein contents, microbial counts and diversity indices. The consortium's strong inhibitory power and adaptability were confirmed by a reduction of STEC levels (average of 2.8 log cfu g(-1)) in all cheeses, whatever the level of STEC inoculated into the milk. Differences in the growth and inhibition of E. coli in the cheeses depended on the microbial composition of the raw milk batches. Further research using a transcriptomic approach will help to improve understanding of the interactions between the strains.

Shiga toxins (Stxs) expressed by the enterohaemorrhagicEscherichia coliand entericShigella dysenteriae 1pathogens are protein synthesis inhibitors. Stxs have been shown to induce apoptosis via the activation of extrinsic and intrinsic pathways in many cell types (epithelial, endothelial, and B cells) but the link between the protein synthesis inhibition and caspase activation is still unclear. Endoplasmic reticulum (ER) stress induced by the inhibition of protein synthesis may be this missing link. Here, we show that the treatment of Burkitt lymphoma (BL) cells with verotoxin-1 (VT-1 or Stx1) consistently induced the ER stress response by activation of IRE1 and ATF6-two ER stress sensors-followed by increased expression of the transcription factor C/REB homologous protein (CHOP). However, our data suggest that, although ER stress is systematically induced by VT-1 in BL cells, its role in cell death appears to be cell specific and can be the opposite: ER stress may enhance VT-1-induced apoptosis through CHOP or play a protective role through ER-phagy, depending on the cell line. Several engineered Stxs are currently under investigation as potential anti-cancer agents. Our results suggest that a better understanding of the signaling pathways induced by Stxs is needed before using them in the clinic.