[CCL19/IL-1beta positive feedback loop involved in the progress of inflammation in rheumatoid arthritis].

Abstract

OBJECTIVE:

To explore the function and mechanism of CCL19 in the pathogenesis of rheumatoid arthritis.

METHODS:

Synovial fibroblasts were collected from 5 cases of rheumatoid arthritis. Peripheral blood mononuclear cells (PBMCs) were obtained from 5 healthy people by Ficoll-Hypaque density gradien centrifugation. The cells were stimulated with IL-1beta, TNF-alpha, IL-17 and other cytokines, and then the expression of CCL19 was detected by RT-PCR. The cells also were treated with different concentration of CCL19, then the expressions of IL-1beta, TNF-alpha were detected by RT-PCR, the expressions of p-ERK, p-p38 were detected by western blot.

RESULTS:

IL-1beta promoted the CCL19/CCR7 expression in both synovial fibroblasts and PBMCs. CCL19 upregulated the expression of IL-10 in both synovial fibroblasts and PBMCs. The stimulation of CCL19 also increased its receptor CCR7 expression. CCL19 activated p-ERK and p-p38 in PBMCs.

CONCLUSION:

The positive feedback loop between CCL19 and IL-1 participate in the development of rheumatoid arthritis.

• Authors: Lian-jie Shi, Jian-hong Li, Xiao-min Cen, Nan-ping Yang, Geng Yin, Qi-bing Xie
• Journal: Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition (Sichuan Da Xue Xue Bao Yi Xue Ban) Vol. 46 Issue 2 Pg. 272-5 (Mar 2015) ISSN: 1672-173X [Print] China
• PMID: 25924444 (Publication Type: Journal Article)

Chemical References

• CCL19 protein, human
• Chemokine CCL19
• IL10 protein, human
• Interleukin-17
• Interleukin-1beta
• Tumor Necrosis Factor-alpha
• Interleukin-10

Topics

• Arthritis, Rheumatoid (physiopathology)
• Cells, Cultured
• Chemokine CCL19 (metabolism)
• Fibroblasts (metabolism)
• Humans
• Inflammation (physiopathology)
• Interleukin-10 (metabolism)
• Interleukin-17 (pharmacology)
• Interleukin-1beta (pharmacology)
• Leukocytes, Mononuclear (metabolism)
• MAP Kinase Signaling System
• Synovial Membrane (cytology)
• Tumor Necrosis Factor-alpha (pharmacology)