AI Article Synopsis
- The study aimed to examine the expression of complement (C) factors and their activation fragments in joint tissues of patients with osteoarthritis (OA) using various biochemical techniques.
- Results indicated that complement factors, particularly C3 and CFB, were expressed mainly in chondrocytes and other joint tissues, with CFB showing a significant increase when stimulated by IL-1β.
- The findings suggest that complement factors are activated in OA joints and play a role in inflammation, highlighting the involvement of innate immunity in the disease process.
Article Abstract
Objective: To investigate complement(C) factors(F) and their activation fragments expression in OA joint tissues.
Design: Immunohistochemistry and quantitative imaging were performed to analyze C3, C4, and CF (factor) B expression on osteochondral biopsies (43 patients) collected during arthroplasty. Isolated chondrocytes and synoviocytes, cartilage and synovial tissues obtained from surgical specimens of OA patients (15 patients) were cultured with or without IL-1β. Real time PCR for CFB, C3, and C4 was performed. Culture supernatants were analyzed for C3a, C5a, CFBa, and terminal complement complex (TCC) production.
Results: In osteochondral biopsies, C factor expression was located in bone marrow, in a few subchondral bone cells and chondrocytes. C3 was the most expressed while factor C4 was the least expressed factor. Gene expression showed that all C factors analyzed were expressed both in chondrocytes and synoviocytes. In chondrocyte cultures and cartilage explants, CFB expression was significantly higher than C3 and C4. Furthermore, CFB, but not C3 and C4 expression was significantly induced by IL-1β. As to C activation factors, C3a was the most produced and CFBa was induced by IL-1β in synovial tissue. TCC production was undetectable in isolated chondrocytes and synoviocytes cell culture supernatants, whereas it was significantly augmented in cartilage explants.
Conclusion: C factors were locally produced and activated in OA joint with the contribution of all tissues (cartilage, bone, and synovium). Our results support the involvement of innate immunity in OA and suggest an association between some C alternative pathway component and joint inflammation.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7658426 | PMC |
| http://dx.doi.org/10.3389/fimmu.2020.535010 | DOI Listing |
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