Effect of PrP105‑132 on the secretion of interleukin‑6 and interleukin‑8 from microglial cells in vitro
Published online on: November 13, 2017
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In the present study, the effect of prion protein (PrP) on the secretion of interleukin‑6 (IL‑6) and IL‑8 from microglial cells in vitro and its possible underlying pathway were investigating by establishing a cell model for prion disease. Rat neuroglial cells were cultured in vitro, and were treated with 80 µM PrP peptides 105‑132 (PrP105‑132) only, PrP+MG132 or PrP+cyclosporin A (CsA). After 48 h, the IL‑6 and IL‑8 levels in the supernatant fluid of the treated cells were detected using enzyme‑linked immunosorbent assay. In addition, the expression levels of nuclear factor‑κB (NF‑κB) and nuclear factor of activated T cells (NFAT) were evaluated using reverse transcription‑polymerase chain reaction. The results indicated that the microglial cells were activated by treatment with PrP peptides. Cell bodies were augmented and appeared to have round, rod and amoeba‑like shapes. In addition, the protuberances were shortened and eventually disappeared. Furthermore, the mRNA expression levels of NF‑κB and NFAT in microglial cells increased, as well as the IL‑6 and IL‑8 levels in the supernatant fluid after treatment with PrP. However, the mRNA expression levels of NF‑κB, and the IL‑6 and IL‑8 levels decreased after these cells were treated with MG132, a specific inhibitor of NF‑κB. The mRNA expression of NFAT decreased after these cells were treated with CsA, a specific inhibitor of NFAT; however, the IL‑6 level decreased, while no significant difference was observed in the IL‑8 level. In conclusion, PrP‑treated microglial cells secreted IL‑6 and IL‑8, and the secretion of IL‑6 was associated with the activation of NF‑κB and NFAT pathways. In addition, the secretion of IL‑8 was mainly dependent on the NF‑κB pathway.