title: Complement contributes to the pathogenesis of Shiga toxin-associated hemolytic uremic syndrome.
abstract: Complement is activated during Shiga toxin-producing Escherichia coli-associated hemolytic uremic syndrome (STEC-HUS). There is evidence of complement activation via the alternative pathway in STEC-HUS patients as well as from in vivo and in vitro models. Ozaki et al. demonstrate activation of the mannose-binding lectin (MBL) pathway in Shiga toxin-treated mice expressing human MBL2, but lacking murine Mbls. Treatment with anti-human MBL2 antibody was protective, suggesting that MBL pathway activation also contributes to Shiga toxin-mediated renal injury.
authors.affiliation: Department of Pediatrics, Clinical Sciences Lund, Lund University, Lund, Sweden. Electronic address: diana.karpman@med.lu.se.
authors.forename: Diana
authors.initials: D
authors.lastname: Karpman
authors.affiliation: Department of Pediatrics, Clinical Sciences Lund, Lund University, Lund, Sweden.
authors.forename: Ramesh
authors.initials: R
authors.lastname: Tati
mesh_terms: D000818:Animals; D004927:Escherichia coli Infections; D006463:Hemolytic-Uremic Syndrome; D006801:Humans; D007668:Kidney; D037601:Mannose-Binding Lectin; D051379:Mice; D022621:Shiga Toxin; D054323:Shiga-Toxigenic Escherichia coli
chemical_list: C445619:MBL2 protein, human; D037601:Mannose-Binding Lectin; D022621:Shiga Toxin