Mechanism of LPS Induced IL-6 Expression in the Growth Arrested Human Mesanigial Cells.
- Author:
Dong Kyu JIN
1
Author Information
1. Department of Pediatrics, Sung Kyun Kwan University, College of Medicine, Samsung Medical Center, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
IL-6;
NF IL-6;
Mesangial cell
- MeSH:
Bacterial Infections;
Cytokines;
Glomerulonephritis;
Humans*;
Inflammation;
Interleukin-6*;
Mesangial Cells
- From:Korean Journal of Nephrology
1997;16(4):642-650
- CountryRepublic of Korea
- Language:English
-
Abstract:
Mesangial cell proliferation contributes to the development of glomerulonephritis and is associated with glomerulosclerosis. It has been reported that IL-6 is a pluri-potent cytokine which is involved in the mesangial inflammation and the activation of IL-6 is related to the recruitment of transcriptional factors or cytokines such as IL-1beta. It has been known that bacterial infection sometimes precedes the exacerbation of glomerulonephritis and bacterial LPS, a potent activator of IL-6, is presumed to be one of the mediators of this inflammatory process. To understand the underlying mechanisms of how IL-6 is activated by LPS, we examined the serial changes of the expression of IL-1beta, IL-6 and NF IL-6(nuclear factor for IL-6) using the growth arrested human mesangial cells at 0, 2, 4, 8, and 18 hours after LPS stimulation. Exposure of serum-free mesangial cells to LPS resulted in the production and the expression of IL-1beta and IL-6. However, there was a steady increase of IL-1b expression throughout the 18 hours, while the peak expression of IL-6 was around 4 hours after LPS stimulation and this peak expression of IL-6 was preceded by NF IL-6. Interestingly, the NF IL-6 expression was not observed in the IL-6 stimulation by r-IL-1beta stimulation. Furthermore, the addition of anti-IL-1beta prior to the LPS stimulation reduced the IL-6 expression partially, but, it did not affect the NF IL-6 expression. These results demonstrated that the mesangial IL-6 expression by LPS is mediated by NF IL-6 as well as IL-1beta in a separate pathways. The capacity of LPS to express IL-6 by these mechanisms may play a role in the mesangial inflammatory process.
