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

Immunobiology
|April 20, 2010
PubMed

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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