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Analyzing the Functions of Mast Cells In Vivo Using 'Mast Cell Knock-in' Mice
Published on: May 27, 2015
Impaired mast cell-dependent natural immunity in complement C3-deficient mice
A P Prodeus1, X Zhou, M Maurer
1Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, USA.
Nature
|November 21, 1997
Summary
Complement activation is crucial for innate immunity, particularly in mast cell-dependent responses. Complement deficiency significantly increases mortality in a model of septic peritonitis, highlighting its essential role.
Area of Science:
- Immunology
- Infectious Disease
Background:
- The complement system is vital for inflammation and mast cell activation.
- Recent studies question complement's role in mast cell-dependent inflammation.
Purpose of the Study:
- To investigate the role of complement in mast cell-dependent natural immunity.
- To examine complement-deficient mice responses to septic peritonitis.
Main Methods:
- Caecal ligation and puncture model in complement-deficient (C4-, C3-) and wild-type (WT) mice.
- Assessed mortality, mast cell degranulation, TNF-alpha production, neutrophil infiltration, and bacterial clearance.
Main Results:
- C4- or C3-deficient mice showed 100% mortality versus 20% in WT mice.
- C3-deficient mice had reduced mast cell degranulation, TNF-alpha production, neutrophil infiltration, and bacterial clearance.
- Supplementation with C3 protein rescued these defects, confirming complement dependence.
Conclusions:
- Complement activation is essential for effective innate immunity in mast cell-dependent bacterial infection models.
- Complement plays a critical role in controlling septic peritonitis through mast cell activation and bacterial clearance.
