Inflammatory synovial fluid microenvironment drives primary human chondrocytes to actively take part in inflammatory joint diseases

Abstract

The role of human chondrocytes in the pathogenesis of cartilage degradation in rheumatic joint diseases has presently gained increasing interest. An active chondrocyte participation in local inflammation may play a role in the initiation and progression of inflammatory joint diseases and in a disruption of cartilage repair mechanisms resulting in cartilage degradation. In the present study, we hypothesized that inflammatory synovial fluid triggers human chondrocytes to actively take part in inflammatory processes in rheumatic joint diseases. Primary human chondrocytes were incubated in synovial fluids gained from patients with rheumatoid arthritis, psoriasis arthritis and reactive arthritis. The detection of vital cell numbers was determined by using Casy Cell Counter System. Apoptosis was measured by Annexin-V and 7AAD staining. Cytokine and chemokine secretion was determined by a multiplex suspension array. Detection of vital cells showed a highly significant decrease in chondrocyte numbers. Flow cytometry demonstrated a significant increase in apoptotic chondrocytes after the incubation. An active secretion of cytokines such as MCP-1 and MIF by chondrocytes was observed. The inflammatory synovial fluid microenvironment mediates apoptosis and cell death of chondrocytes. Moreover, in terms of cytokine secretion, it also induces an active participation of chondrocytes in ongoing inflammation.

Prolactin promotes cartilage survival and attenuates inflammation in inflammatory arthritis

“…Cyt concentrations were similar to those (1-10 ng/ml) found in synovial fluid of patients with RA with severe disease activity (34,35) or produced by activated chondrocytes (36). PRL opposed the Cyt proapoptotic effect in a dose-dependent manner at concentrations (0.2-2.3 μg/ml) higher than those reported in RA synovial fluid (0.007-0.02 μg/ml) (14, 15) but similar to those (0.2-0.3 μg/ml) circulating in pregnancy and lactation (37).…”

Cytokine Levels (IL-4, IL-6, IL-8 and TGFβ) as Potential Biomarkers of Systemic Inflammatory Response in Trauma Patients

“…According to previous findings that certain pro-inflammatory cytokines, such as IL-6, may cause or intensify psychological symptoms [27], these results suggest that high levels of inflammation due to injury may be a risk factor for post trauma psychological symptomatology. Other studies described other conditions with significant levels of various cytokines in the synovial fluid of patients with rheumatoid arthritis and also in patients with osteoarthritis, supporting a pro-inflammatory process in the pathogenesis of osteoarthritis [28][29][30]. Elevated plasma levels of proinflammatory cytokines, such as IL-1beta, IL-8 and TNFalpha, were also observed as useful markers of bone resorption in patients with aseptic loosening of large joint prosthesis [31].…”

Osteoarthritis synovial fluid activates pro-inflammatory cytokines in primary human chondrocytes

“…In a recent study, we were able to show an active participation of human chondrocytes in inflammatory processes [7]. Here, we intended to investigate the behavior of human chondrocytes in a non-inflammatory environment, as is supposed to be found in the degenerative disease osteoarthritis.…”

“…In a recent study, we could demonstrate that inflammatory synovial fluids of patients with reactive arthritis, psoriasis arthritis or RA mediate apoptosis and cell death of chondrocytes. Furthermore, inflammatory cytokine secretion in human chondrocytes was shown [7].…”