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Published on: May 2, 2017
Properdin deficiency in murine models of nonseptic shock
Nina D Ivanovska1, Petya A Dimitrova, Jeni C Luckett
1Department of Immunology, Institute of Microbiology, Bulgarian Academy of Sciences, Sofia, Bulgaria.
Abstract:
Hereditary properdin deficiency is linked to susceptibility to meningococcal disease (Neisseria meningitidis serotypes Y and W-135) with high mortality. Its relative contribution toward the outcome of nonseptic shock has not been investigated. Using properdin-deficient C57BL/6 mice and their littermates, this study examines their survival of zymosan-induced and LPS-induced shock. Properdin-deficient mice were more resistant to zymosan shock compared with wild-type mice, which showed greater impairment of end-organ function 24 h after zymosan injection, higher TNF-alpha production by alveolar and peritoneal macrophages, higher TNF-alpha, and, inversely, lower IL-10 levels in peritoneal lavage and circulation and higher plasma C5a levels. Properdin-deficient mice showed significantly higher mortality in LPS shock, elevated TNF-alpha, and, inversely, reduced IL-10 production by peritoneal macrophages as well as lower plasma C5a levels compared with wild-type littermates. NO production by peritoneal macrophages and plasma alpha1-antitrypsin levels at 24 h after the injection of LPS or zymosan were decreased in properdin-deficient mice in both models, and fewer histopathologic changes in liver were observed in properdin-deficient animals. This study provides evidence that properdin deficiency attenuates zymosan-induced shock and exacerbates LPS-induced shock.
Insights
Properdin deficiency protects against zymosan shock but worsens lipopolysaccharide (LPS)-induced shock. This study investigated properdin
Area of Science:
- Immunology
- Complement System Biology
- Pathophysiology
Background:
- Hereditary properdin deficiency increases susceptibility to meningococcal disease.
- The role of properdin in nonseptic shock remains unclear.
- Properdin is a key component of the alternative complement pathway.
Purpose of the Study:
- To investigate the role of properdin in zymosan-induced and lipopolysaccharide (LPS)-induced shock.
- To examine the impact of properdin deficiency on survival, end-organ function, and inflammatory responses in mouse models of shock.
Main Methods:
- Utilized properdin-deficient and wild-type C57BL/6 mice.
- Administered zymosan or LPS to induce shock.
- Assessed survival rates, end-organ function, cytokine (TNF-alpha, IL-10) production, complement component (C5a) levels, nitric oxide (NO) production, and liver histopathology.
Main Results:
- Properdin-deficient mice exhibited increased resistance to zymosan shock but higher mortality in LPS shock.
- Zymosan shock in properdin-deficient mice showed reduced TNF-alpha and increased IL-10, with lower C5a levels.
- LPS shock in properdin-deficient mice displayed elevated TNF-alpha, reduced IL-10, and lower C5a levels, alongside decreased NO production and fewer liver histopathologic changes.
Conclusions:
- Properdin deficiency differentially affects outcomes in experimental shock models.
- Properdin plays a protective role in zymosan-induced shock but a detrimental role in LPS-induced shock.
- Findings highlight the complex involvement of properdin in inflammatory shock pathophysiology.
