| Literature DB >> 26704184 |
Yuanqiang Zhang1, Lian Liu1, Shuaishuai Wang1, Yunpeng Zhao1, Yi Liu1, Jingkun Li1, Lin Nie1, Lei Cheng2.
Abstract
IL-17-producing cells play an important role in various autoimmune diseases. A higher level of IL-17-producing cells is observed in patients with intervertebral disc (IVD) degeneration. However, the mechanism of the accumulation of IL-17-producing cells remains to be elucidated. Our aim is to demonstrate whether the interaction of CC chemokine ligand (CCL) 20 and its specific receptor CCR6 is involved in the recruitment of IL-17-producing cells to degenerated disc tissues in rat models. The well-accepted needle puncture model and the autologous nucleus pulposus application model of rats were established. All of the animals were randomly divided into four groups: the sham surgery group, the needle puncture group (NP group), the sham surgery + autologous nucleus pulposus application group (sham-ANPA group) and the needle puncture + autologous nucleus pulposus application group (NP-ANPA group). Immunohistochemical staining, western blot and real-time PCR were used to evaluate the expression levels of CCL20, IL-17 and CCR6 in the IVD samples. Moreover, the IL-17 concentrations in the serum were detected by ELISA. Pearson correlations were performed to analyse the correlation among the expressions of CCL20, CCR6 and IL-17. The expressions of CCL20, IL17 and CCR6 were dramatically elevated in comparison with the control groups. The circulating IL-17 in the serum of the NP-ANPA group was elevated compared to the sham surgery group. In addition, there was a positive correlation among the expression levels of CCL20, CCR6 and IL-17. The results suggest a potential mechanism for the recruitment of IL-17-producing cells to degenerated intervertebral discs via a CCL20/CCR6 system in vivo.Entities:
Keywords: CC chemokine ligand 20; CC chemokine receptor 6; Degenerated intervertebral discs; Interleukin-17; Nucleus pulposus; Rats
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Year: 2015 PMID: 26704184 DOI: 10.1007/s10735-015-9651-2
Source DB: PubMed Journal: J Mol Histol ISSN: 1567-2379 Impact factor: 2.611