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Published on: December 16, 2021
Complement system becomes activated by the classical pathway in intracranial aneurysm walls.
Riikka Tulamo1, Juhana Frösen, Sami Junnikkala
1Neurosurgery Research Group, Biomedicum Helsinki, Helsinki, Huch FI-00029, Finland. riikka.tulamo@hus.fi
Laboratory Investigation; a Journal of Technical Methods and Pathology
|December 10, 2009
Summary
Complement activation via the classical pathway in intracranial aneurysms (IAs) involves multiple factors and lipids, indicating chronic inflammation. This process, linked to IA rupture, may stem from impaired complement regulation under stress.
Area of Science:
- Vascular Biology
- Immunology
- Pathology
Background:
- Intracranial aneurysm (IA) rupture is linked to inflammation and complement system activation within the IA wall.
- Previous studies show C5b-9 accumulation correlates with IA rupture and wall degeneration.
Purpose of the Study:
- To investigate the initiators and pathways of complement activation in unruptured and ruptured intracranial aneurysms.
- To elucidate the mechanisms underlying complement-mediated inflammation in IA pathogenesis.
Main Methods:
- Immunohistochemical and immunofluorescence staining of IA wall samples (unruptured and ruptured).
- Analysis of classical and alternative complement pathway components, putative activators (IgG, IgM, CRP, OxLDL), and C5b-9.
- Oil-Red-O staining for lipid localization.
Main Results:
- Classical complement pathway components were present in all IAs, primarily in the extracellular matrix.
- Complement component accumulation areas were significantly larger in ruptured IAs compared to unruptured ones.
- C5b-9 colocalized with lipids in the extracellular matrix, suggesting a chronic inflammatory process.
Conclusions:
- Complement activation in IA walls occurs via the classical pathway, induced by multiple factors including immunoglobulins, CRP, OxLDL, and potentially vascular pressure.
- The terminal pathway activation focuses on lipid-rich areas, indicating a chronic inflammatory response.
- Impaired local complement regulation under stress may contribute to IA wall degeneration and rupture.
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