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Modulatory effect of rhein on IL-1alpha-induced responses in human chondrocytes: a comparative study between antibody
J Deffaud1, M Kirchmeyer, F Domagala
1UMR 7561 CNRS-Nancy-Université, Laboratoire de Physiopathologie & Pharmacologie Articulaires (LPPA), Vandoeuvre-lès-Nancy, France.
Abstract:
The present work aimed to take advantage of the screening capacity of protein arrays to search for additional targets of rhein in interleukin (IL)-1-stimulated chondrocytes. Primary cultures of chondrocytes from osteoarthritic (OA) patients were stimulated for 24 and 48 h with 1 ng/ml of IL-1alpha, in the presence or absence of 10(-5) M of rhein. Culture supernatants were analyzed with arrays membranes consisting of 120 antibodies directed against cytokines, chemokines, and angiogenic or growth factors and were controlled for 8 proteins by specific immuno-enzymatic assays (ELISA). Protein arrays showed that several CC or CXC chemokines, the growth factor GM-CSF, the cytokines IL-6, IL-7 and IL-10 (but unexpectedly not IL-1beta or TNFalpha) and the adhesion molecule ICAM-1 were induced maximally by IL-1alpha. In IL-1-stimulated chondrocytes, rhein reduced slightly the production of MCP-1 and increased those of IL-1Ra, of the cytokine receptors sgp130, IL-6R, sTNFR I and R II, but also of some chemokines or ICAM-1. Specific ELISAs confirmed the effect of rhein on MCP-1, IL-1Ra, sgp130, IL-6R and sTNFR II but was discrepant for GROalpha and were always more sensitive than protein arrays to detect IL-1 effects such as IL-1Ra and TNFalpha release. The present data show that rhein modulated some IL-1-induced responses contributing possibly to its chondroprotective (IL-1Ra, MCP-1) or cytokine modifying (sTNFR II, sgp130) properties, but that protein arrays were poorly sensitive to check for IL-1- and/or rhein-induced changes.
Insights
Rhein, a compound studied for osteoarthritis, modulated interleukin-1 responses in chondrocytes. It reduced some inflammatory markers and increased protective ones, though protein arrays had limitations in detecting these changes.
Area of Science:
- Biochemistry
- Immunology
- Cell Biology
Background:
- Osteoarthritis (OA) involves inflammation in chondrocytes.
- Interleukin-1 (IL-1) is a key inflammatory mediator in OA.
- Rhein is a compound with potential therapeutic properties in OA.
Purpose of the Study:
- To identify additional molecular targets of rhein in IL-1-stimulated chondrocytes using protein arrays.
- To investigate the effects of rhein on IL-1-induced cytokine and chemokine production in OA chondrocytes.
Main Methods:
- Primary chondrocytes from OA patients were stimulated with IL-1alpha and rhein.
- Culture supernatants were analyzed using protein arrays (120 antibodies) and ELISA.
- Detected proteins included cytokines, chemokines, growth factors, and adhesion molecules.
Main Results:
- IL-1alpha induced several proteins, including chemokines, GM-CSF, IL-6, IL-7, IL-10, and ICAM-1.
- Rhein reduced MCP-1 and increased IL-1Ra, cytokine receptors (sgp130, IL-6R), and TNFRs.
- ELISAs confirmed rhein's effects on MCP-1, IL-1Ra, sgp130, IL-6R, and sTNFR II, but protein arrays showed limited sensitivity.
Conclusions:
- Rhein modulates IL-1-induced responses in chondrocytes, potentially contributing to chondroprotection (e.g., via IL-1Ra, MCP-1) and cytokine modification (e.g., sTNFR II, sgp130).
- Protein arrays demonstrated lower sensitivity for detecting IL-1 and rhein-induced changes compared to specific ELISAs.
