ArticleBMC microbiology2015
The secreted autotransporter toxin (Sat) does not act as a virulence factor in the probiotic Escherichia coli strain Nissle 1917.
Article in BMC microbiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- A next-generation probiotic strain for gut health: Bacteroides cellulosilyticus LYH2 variant with anti-inflammatory and metabolic advantages.EBioMedicine · 2026Article
- Secreted autotransporter toxin produced by probioticmicroPublication biology · 2025Article
- The Next-Generation ProbioticNutrients · 2024Article
- Diagnosis of extraintestinal pathogenicCurrent research in microbial sciences · 2024Review
- Gastrointestinal dysbiosis and Escherichia coli pathobionts in inflammatory bowel diseases.APMIS : acta pathologica, microbiologica, et immunologica Scandinavica · 2022Article
- Supplementation of Labneh with Passion Fruit Peel Enhanced Survival ofFoods (Basel, Switzerland) · 2022Article
- Secreted Autotransporter Toxin (Sat) Mediates Innate Immune System Evasion.Frontiers in immunology · 2022Article
- Microbiota-derived extracellular vesicles in interkingdom communication in the gut.Journal of extracellular vesicles · 2021Review
- Looking into key bacterial proteins involved in gut dysbiosis.World journal of methodology · 2021Review
- Investigation of CommensalMicroorganisms · 2021Article
- Heparin stimulates biofilm formation of Escherichia coli strain Nissle 1917.Biotechnology letters · 2021Article
- Probiotic Escherichia coli Nissle 1917-derived outer membrane vesicles enhance immunomodulation and antimicrobial activity in RAW264.7 macrophages.BMC microbiology · 2020Article
- Secreted autotransporter toxin (Sat) induces cell damage during enteroaggregative Escherichia coli infection.PloS one · 2020Article
- Serine Protease Autotransporters of theMicroorganisms · 2019Review
- Extracellular vesicles and soluble factors secreted by Escherichia coli Nissle 1917 and ECOR63 protect against enteropathogenic E. coli-induced intestinal epithelial barrier dysfunction.BMC microbiology · 2019Article
- K5 Capsule and Lipopolysaccharide Are Important in Resistance to T4 Phage Attack in ProbioticFrontiers in microbiology · 2019Article
- Outer Membrane Vesicles and Soluble Factors Released by ProbioticFrontiers in microbiology · 2016Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEscherichia coli Nissle 1917 (EcN) is a probiotic used in the treatment of intestinal diseases. Although it is considered safe, EcN is closely related to the uropathogenic E. coli strain CFT073 and contains many of its predicted virulence elements. Thus, it is relevant to assess whether virulence-associated genes are functional in EcN. One of these genes encodes the secreted autotransporter toxin (Sat), a member of the serine protease autotransporters of Enterobacteriaceae (SPATEs) that are secreted following the type V autotransporter pathway. Sat is highly prevalent in certain E. coli pathogenic groups responsible for urinary and intestinal infections. In these pathogens Sat promotes cytotoxic effects in several lines of undifferentiated epithelial cells, but not in differentiated Caco-2 cells.
resultsHere we provide evidence that sat is expressed by EcN during the colonization of mouse intestine. The EcN protein is secreted as an active serine protease, with its 107 kDa-passenger domain released into the medium as a soluble protein. Expression of recombinant EcN Sat protein in strain HB101 increases paracellular permeability to mannitol in polarized Caco-2 monolayers. This effect, also reported for the Sat protein of diffusely adherent E. coli, is not observed when this protein is expressed in the EcN background. In addition, we show that EcN supernatants confer protection against Sat-mediated effects on paracellular permeability, thus indicating that other secreted EcN factors are able to prevent barrier disruption caused by pathogen-related factors. Sat is not required for intestinal colonization, but the EcNsat::cat mutant outcompetes wild-type EcN in the streptomycin-treated mouse model. Analysis of the presence of sat in 29 strains of the ECOR collection isolated from stools of healthy humans shows 34.8 % positives, with high prevalence of strains of the phylogenetic groups D and B2, related with extra-intestinal infections.
conclusionsSat does not act as a virulence factor in EcN. The role of Sat in intestinal pathogenesis relies on other genetic determinants responsible for the bacterial pathotype.
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