ArticleKidney international2016
Human mannose-binding lectin inhibitor prevents Shiga toxin-induced renal injury.
Article in Kidney international, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- Role of CD4+ T cell mannose binding lectin in Schistosoma-induced pulmonary hypertension.JCI insight · 2026Article
- Antibodies to mannose-binding lectin and factor XI Inhibit Shiga toxin-induced kidney injury additively in a murine model.Pediatric research · 2026Article
- The Role of the Complement System in the Pathogenesis of Infectious Forms of Hemolytic Uremic Syndrome.Biomolecules · 2023Review
- Shiga toxin targets the podocyte causing hemolytic uremic syndrome through endothelial complement activation.Med (New York, N.Y.) · 2023Article
- The Diagnostic Significance of C3d Antigen in Kidney and Skin Histopathology - The Current State-Of-The-Art and Practical Examples.Physiological research · 2023Review
- Diagnosis and Treatment for Shiga Toxin-ProducingToxins · 2022Review
- α2,6-Sialylation Is Upregulated in Severe COVID-19, Implicating the Complement Cascade.ACS infectious diseases · 2022Article
- α2,6-Sialylation is Upregulated in Severe COVID-19 Implicating the Complement Cascade.medRxiv : the preprint server for health sciences · 2022Article
- A clinical approach to children with C3 glomerulopathy.Pediatric nephrology (Berlin, Germany) · 2022Review
- The Syndromes of Thrombotic Microangiopathy: A Critical Appraisal on Complement Dysregulation.Journal of clinical medicine · 2021Review
- A Plausible Role for Collectins in Skin Immune Homeostasis.Frontiers in immunology · 2021Review
- Ex vivo assays to detect complement activation in complementopathies.Clinical immunology (Orlando, Fla.) · 2020Article
- Shiga toxin triggers endothelial and podocyte injury: the role of complement activation.Pediatric nephrology (Berlin, Germany) · 2019Review
- Complement Activation Contributes to the Pathophysiology of Shiga Toxin-Associated Hemolytic Uremic Syndrome.Microorganisms · 2019Review
- Article
- Haemolytic uremic syndrome: diagnosis and management.F1000Research · 2019Review
- Advances in our understanding of the pathogenesis of hemolytic uremic syndromes.American journal of physiology. Renal physiology · 2018Review
- Review
- Complement C5-inhibiting therapy for the thrombotic microangiopathies: accumulating evidence, but not a panacea.Clinical kidney journal · 2017Article
- HUS and atypical HUS.Blood · 2017Review
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Authors and funding
11 authors at 3 institutions in 3 countries.
Funding
Abstract
Hemolytic uremic syndrome caused by Shiga toxin-producing Escherichia coli (STEC HUS) is a worldwide endemic problem, and its pathophysiology is not fully elucidated. Here we tested whether the mannose-binding lectin (MBL2), an initiating factor of lectin complement pathway activation, plays a crucial role in STEC HUS. Using novel human MBL2-expressing mice (MBL2 KI) that lack murine Mbls (MBL2(+/+)Mbl1(-/-)Mbl2(-/-)), a novel STEC HUS model consisted of an intraperitoneal injection with Shiga toxin-2 (Stx-2) with or without anti-MBL2 antibody (3F8, intraperitoneal). Stx-2 induced weight loss, anemia, and thrombocytopenia and increased serum creatinine, free serum hemoglobin, and cystatin C levels, but a significantly decreased glomerular filtration rate compared with control/sham mice. Immunohistochemical staining revealed renal C3d deposition and fibrin deposition in glomeruli in Stx-2-injected mice. Treatment with 3F8 completely inhibited serum MBL2 levels and significantly attenuated Stx-2 induced-renal injury, free serum hemoglobin levels, renal C3d, and fibrin deposition and preserved the glomerular filtration rate. Thus, MBL2 inhibition significantly protected against complement activation and renal injury induced by Stx-2. This novel mouse model can be used to study the role of complement, particularly lectin pathway-mediated complement activation, in Stx-2-induced renal injury.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.