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


CONCLUSIONS
The positive feedback loop between CCL19 and IL-1 participate in the development of rheumatoid arthritis.
Lian-jie
LJ
Shi
Jian-hong
JH
Li
Xiao-min
XM
Cen
Nan-ping
NP
Yang
Geng
G
Yin
Qi-bing
QB
Xie
D001172:Arthritis, Rheumatoid / Q000503:physiopathology*; D002478:Cells, Cultured; D054415:Chemokine CCL19 / Q000378:metabolism*; D005347:Fibroblasts / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000503:physiopathology*; D016753:Interleukin-10 / Q000378:metabolism; D020381:Interleukin-17 / Q000494:pharmacology; D053583:Interleukin-1beta / Q000494:pharmacology*; D007963:Leukocytes, Mononuclear / Q000378:metabolism; D020935:MAP Kinase Signaling System; D013583:Synovial Membrane / Q000166:cytology; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
C515460:CCL19 protein, human; D054415:Chemokine CCL19; C508609:IL10 protein, human; D020381:Interleukin-17; D053583:Interleukin-1beta; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10