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Updated: Jun 13, 2026

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation
Published on: May 23, 2025
Mannose-binding lectin and its associated proteases (MASPs) mediate coagulation and its deficiency is a risk factor
Kazue Takahashi1, Wei-Chuan Chang, Minoru Takahashi
1Developmental Immunology Program, Department of Pediatrics, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA. ktakahashi1@partners.org
Abstract:
The first line of host defense is the innate immune system that includes coagulation factors and pattern recognition molecules, one of which is mannose-binding lectin (MBL). Previous studies have demonstrated that MBL deficiency increases susceptibility to infection. Several mechanisms are associated with increased susceptibility to infection, including reduced opsonophagocytic killing and reduced lectin complement pathway activation. In this study, we demonstrate that MBL and MBL-associated serine protease (MASP)-1/3 together mediate coagulation factor-like activities, including thrombin-like activity. MBL and/or MASP-1/3 deficient hosts demonstrate in vivo evidence that MBL and MASP-1/3 are involved with hemostasis following injury. Staphylococcus aureus infected MBL null mice developed disseminated intravascular coagulation (DIC), which was associated with elevated blood IL-6 levels (but not TNF-α and multi-organ inflammatory responses). Infected MBL null mice also develop liver injury. These findings suggest that MBL deficiency may manifest into DIC and organ failure during infectious diseases.
Insights
Mannose-binding lectin (MBL) deficiency impairs host defense, increasing infection susceptibility. This study reveals MBL
Area of Science:
- Immunology
- Infectious Diseases
- Hematology
Background:
- The innate immune system, including mannose-binding lectin (MBL), is crucial for host defense against infection.
- MBL deficiency is linked to increased susceptibility to infections via impaired opsonophagocytosis and complement activation.
- The role of MBL in hemostasis and its connection to coagulation factors remain incompletely understood.
Purpose of the Study:
- To investigate the role of MBL and MBL-associated serine proteases (MASPs) in coagulation and hemostasis.
- To examine the consequences of MBL deficiency in a mouse model of Staphylococcus aureus infection, focusing on hemostasis and organ injury.
Main Methods:
- Assessed coagulation factor-like activities of MBL and MASP-1/3 complexes.
- Utilized MBL-deficient mice to study hemostasis following injury in vivo.
- Infected MBL-null mice with Staphylococcus aureus to evaluate disseminated intravascular coagulation (DIC) and organ damage.
Main Results:
- MBL and MASP-1/3 exhibit thrombin-like activity, suggesting a role in coagulation.
- MBL and MASP-1/3 deficient hosts show impaired hemostasis post-injury.
- MBL-null mice infected with S. aureus developed DIC, elevated IL-6, and liver injury.
Conclusions:
- MBL and MASP-1/3 play a significant role in mediating coagulation-like activities and hemostasis.
- MBL deficiency can lead to disseminated intravascular coagulation (DIC) and organ failure during infectious disease, particularly S. aureus infections.
- These findings highlight a critical link between the innate immune system, coagulation, and infectious disease pathogenesis.
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