Activating Compound | Comment | Organism | Structure |
---|---|---|---|
additional information | inflammatory mediators such as bacterial lipopolysaccharide and polymorphonuclear neutrophils contribute to hemolytic-uremic syndrome pathophysiology by potentiating Stx effects in human astrocytes. Inhibition of NF-kappaB or blockade of TNF-alpha activity abrogates effects mediated by Stx1 in lipopolysaccharide-sensitized astrocytes | Escherichia coli |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Escherichia coli | - |
Shiga-toxin producing strains | - |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
additional information | Stx1 binding and internalization in L929 human host cells, and cytotoxicity, overview | Escherichia coli | - |
Synonyms | Comment | Organism |
---|---|---|
Shiga toxin 1 | - |
Escherichia coli |
Stx type 1 | - |
Escherichia coli |
Stx1 | - |
Escherichia coli |
General Information | Comment | Organism |
---|---|---|
malfunction | hemolytic-uremic syndrome is generally caused by Shiga toxin-producing Escherichia coli. Endothelial dysfunction mediated by Stx is a central aspect in hemolytic-uremic syndrome development. Inflammatory mediators such as bacterial lipopolysaccharide and polymorphonuclear neutrophils contribute to HUS pathophysiology by potentiating Stx effects, pathology, overview | Escherichia coli |