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[Inhibitory effect of interleukin-10 on inflammatory reaction in rat mesangial cells]
Insights
Interleukin-10 (IL-10) significantly reduces inflammatory responses in rat mesangial cells (rMC). This cytokine inhibits cell proliferation and the production of key inflammatory mediators like IL-1 and TNF-alpha.
Area of Science:
- Nephrology
- Immunology
- Cell Biology
Context:
- Glomerular mesangial cells (rMC) play a crucial role in kidney inflammation.
- Inflammatory mediators such as IL-1 and TNF alpha contribute to glomerular injury.
- Intercellular adhesion molecule-1 (ICAM-1) is involved in inflammatory cell recruitment in the glomerulus.
Purpose:
- To investigate the inhibitory effect of Interleukin-10 (IL-10) on inflammatory reactions in rat mesangial cells (rMC).
Summary:
- IL-10 significantly inhibited both fetal calf serum (FCS) and IL-1-induced proliferation of rMC.
- IL-10 suppressed the bioactivity and gene expression of IL-1 and TNF alpha in rMC.
- Treatment with IL-10 attenuated the IL-1-induced expression of ICAM-1 on rMC surface.
Impact:
- IL-10 demonstrates potential as an inhibitory cytokine in regulating glomerular inflammation.
- Findings suggest IL-10's role in managing inflammatory conditions affecting mesangial cells.
- This research contributes to understanding cytokine-mediated regulation of kidney inflammation.
Objective:
To investigate the inhibitory effect of IL-10 on inflammatory reaction in rat mesangial cells (rMC).
Methods:
Cell proliferation was tested by 3H-thymidine uptake and absolute cell counts. The production of IL-1 and TNF alpha by rMC was assessed by bioactivity assay and their gene expression by Northern blot hybridization. The expression of intercellular adhesion molecule-1 (ICAM-1) on rMC was determined by ELISA.
Results:
IL-10 (25 ng/ml) inhibited 5% FCS and IL-1 induced cell proliferation by 39% and 52% respectively. It also suppressed the production of IL-1 and TNF alpha bioactivity by rMC by 48% and 68%, which was consistent with the decline of IL-1 and TNF alpha gene expression. The IL-1-induced expression of ICAM-1 on surface of rMC was attenuated by IL-10 treatment.
Conclusion:
Our data suggest that IL-10 may be an inhibitory cytokine in regulation of inflammatory reaction in glomerular mesangial cells.