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Published on: June 8, 2022
Marasmius oreades lectin induces renal thrombotic microangiopathic lesions
Roscoe L Warner1, Harry C Winter, Cecilia L Speyer
1Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109-0602, USA.
Abstract:
The present studies demonstrate that infusion of a type B specific lectin derived from the mushroom Marasmius oreades (MOA) into mice binds selectively to the glomerular endothelial cells via surface carbohydrate moieties resulting in cell injury and death associated with platelet-fibrin thrombi. This selective MOA binding to the endothelial cells can be abrogated by a sugar specific for the carbohydrate sequence. Hemolytic-Uremic Syndrome (HUS) and the closely associated Thrombotic Thrombocytopenic Purpura (TTP) are diseases associated with widespread microvascular injury in various organs. Clinically, these diseases are associated with microangiopathic hemolytic anemia and thrombocytopenia. The kidney glomerulus is a primary target of this microvascular injury. There are many underlying etiologies including bacterial toxins. Experimentally, such toxins injure endothelial cells in vitro but in vivo studies have failed to reproduce the characteristic renal pathology. We suggest that MOA-induced glomerular microangiopathic injury could be used to study the pathophysiology of endothelial cell injury as related to glomerular microangiopathic injury.
Insights
Mushroom lectin MOA selectively injures mouse kidney cells, causing thrombi. This model could advance understanding of diseases like Hemolytic-Uremic Syndrome (HUS) and Thrombotic Thrombocytopenic Purpura (TTP).
Area of Science:
- Nephrology
- Toxicology
- Immunology
Background:
- Hemolytic-Uremic Syndrome (HUS) and Thrombotic Thrombocytopenic Purpura (TTP) involve microvascular injury, primarily affecting kidney glomeruli.
- Bacterial toxins cause endothelial cell injury in vitro, but in vivo models struggle to replicate renal pathology.
Purpose of the Study:
- To investigate the potential of a mushroom-derived lectin, Marasmius oreades agglutinin (MOA), as a model for studying glomerular microangiopathic injury.
- To explore the mechanism of MOA-induced endothelial cell damage and thrombus formation in vivo.
Main Methods:
- Infusion of type B specific lectin (MOA) from Marasmius oreades into mice.
- Observation of MOA binding to glomerular endothelial cells and subsequent cell injury and death.
- Assessment of platelet-fibrin thrombi formation.
- Testing the abrogation of MOA binding using a specific sugar.
Main Results:
- MOA selectively binds to glomerular endothelial cells via surface carbohydrates, leading to cell injury and death.
- Platelet-fibrin thrombi were observed in association with MOA-induced endothelial damage.
- Specific sugar molecules successfully abrogated MOA binding to endothelial cells.
Conclusions:
- MOA induces selective glomerular microangiopathic injury in mice.
- This MOA-induced injury model offers a novel approach to study the pathophysiology of endothelial cell damage relevant to HUS and TTP.
- The findings highlight the role of specific carbohydrate-lectin interactions in microvascular injury.
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