Related Experiment Videos
Complement in acute and chronic arthritides: assessment of C3c, C9, and protectin (CD59) in synovial membrane
Y T Konttinen1, A Ceponis, S Meri
1Department of Medicine, Helsinki University of Central Hospital, Finland.
Insights
Complement activation in rheumatoid arthritis and acute arthritides correlates with reduced protection of synovial cells. This suggests a mechanism for complement-mediated damage in inflammatory joint diseases.
Area of Science:
- Immunology
- Rheumatology
- Cell Biology
Background:
- The complement system plays a crucial role in immune responses.
- Understanding complement's role in arthritis is vital for developing targeted therapies.
- Dysregulation of complement can lead to tissue damage in inflammatory conditions.
Purpose of the Study:
- To compare complement cascade activation and protection in acute arthritides versus rheumatoid arthritis.
- To investigate the expression of complement components and protectin in various joint conditions.
- To elucidate the relationship between complement-mediated damage and cellular protection in synovial tissues.
Main Methods:
- Avidin-biotin-peroxidase complex staining was used to detect C3c, C9, and protectin (CD59).
- Immunohistochemical analysis was performed on synovial tissue samples.
- Comparison of marker expression across rheumatoid arthritis, acute arthritides, and chronic joint derangements.
Main Results:
- Significant deposits of C3c and C9 were observed in rheumatoid arthritis and acute arthritides.
- Protectin (CD59) expression was notably weak in synovial lining, stromal, and endothelial cells in these inflammatory conditions.
- Conversely, C3c and C9 deposits were absent, and protectin expression was prominent in chronic degenerative or mechanical joint diseases.
Conclusions:
- Complement activation in rheumatoid arthritis and acute arthritides is linked to diminished protectin-mediated defense of synovial cells.
- This suggests that reduced protection against the membrane attack complex contributes to joint damage in these conditions.
- The findings highlight a potential therapeutic target for mitigating complement-induced injury in inflammatory arthritis.
Objectives:
To investigate the role of complement cascade induced damage and protection against it in acute arthritides compared to rheumatoid arthritis and other chronic joint derangements.
Methods:
C3c, C9, and protectin (CD59) were examined by avidin-biotin-peroxidase complex staining.
Results:
Marked deposits of C3c and C9 were found in synovial vasculature and intercellular matrix of the lining in rheumatoid arthritis and in acute arthritides (including bacterial, reactive, and osteoarthritis flare up). Furthermore, protectin was not visible in synovial lining cells and was relatively weakly expressed in stromal and endothelial cells in rheumatoid arthritis; also in acute arthritides protectin expression was weak. In contrast, C3c and C9 deposits were not found in chronic conditions associated with degenerative diseases (osteoarthritis and osteochondritis dissecans) or mechanical causes (patellar luxation and a ruptured meniscus), in which also the protectin expression was prominent in synovial lining, endothelial and some stromal cells.
Conclusions:
Activation of the complement in rheumatoid arthritis and in acute arthritides seems to be associated with a decreased protection of synovial cells against cellular effects and lysis mediated by membrane attack complex.