Department of Neurology, University of Texas-Houston, Health Science Center, 6431 Fannin St., Houston, TX 77030, United States.
Cytokine. 2013 Jan;61(1):323-8. doi: 10.1016/j.cyto.2012.10.015. Epub 2012 Nov 11.
Ingested immunoactive proteins type I IFN, SIRS peptide 1-21, α-MSH, ACTH, SST inhibit clinical attacks and inflammation in acute EAE by decreasing Th1-like cytokines, increasing Th2-like cytokines or increasing T(reg) cell frequencies.
We examined whether another protein, thyrotropin releasing factor (TRH), would have similar anti-inflammatory effects in EAE after oral administration.
DESIGN/METHODS: B6 mice were immunized with MOG peptide 35-55 and gavaged with control saline or TRH during ongoing disease. Splenocytes from mock fed or TRH fed mice were adoptively transferred into active MOG peptide 35-55 immunized recipient mice during ongoing disease.
Ingested (oral) TRH inhibited ongoing disease and decreased inflammation. Adoptively transferred cells from TRH fed donors protected against actively induced disease and decreased inflammation. In actively fed mice, oral TRH decreased IL-17 and TNF-α cytokines in both the spleen and the CNS. In recipients of donor cells from TRH fed mice there was a reduction of Th1 and Th17 and induction of Th2-like IL-13 cytokines in both the spleen and CNS. Oral TRH decreased clinical score and decreased inflammatory foci in both actively fed and recipients of actively fed mice. There was no significant increase in T(reg) cell frequencies in actively fed or recipients of TRH fed donor cells.
Ingested (orally administered) TRH can inhibit clinical disease, inhibit CNS inflammation by decreasing Th1-like, Th17 and TNF-α cytokines and increasing Th2-like cytokines (IL-13) in the CNS.
摄入具有免疫活性的蛋白质 I 型干扰素、SIRS 肽 1-21、α-MSH、ACTH、SST 可通过降低 Th1 样细胞因子、增加 Th2 样细胞因子或增加 T(reg)细胞频率来抑制急性 EAE 中的临床发作和炎症。
我们研究了另一种蛋白质促甲状腺激素释放因子 (TRH) 在口服后是否对 EAE 具有类似的抗炎作用。
设计/方法：B6 小鼠用 MOG 肽 35-55 免疫，并在疾病进展期间用对照盐水或 TRH 灌胃。来自模拟喂养或 TRH 喂养小鼠的脾细胞在疾病进展期间被过继转移到正在接受主动 MOG 肽 35-55 免疫的受体小鼠中。
摄入（口服）TRH 可抑制进行性疾病并减少炎症。来自 TRH 喂养供体的过继转移细胞可预防主动诱导的疾病并减少炎症。在主动喂养的小鼠中，口服 TRH 可降低脾脏和中枢神经系统中的 IL-17 和 TNF-α 细胞因子。在接受来自 TRH 喂养供体的细胞的受体小鼠中，脾和中枢神经系统中 Th1 和 Th17 减少，Th2 样 IL-13 细胞因子增加。口服 TRH 可降低主动喂养和接受主动喂养的小鼠受体的临床评分，并减少炎症灶。在主动喂养或接受 TRH 喂养供体细胞的受体中，T(reg)细胞频率没有明显增加。
摄入（口服给予）TRH 可抑制临床疾病，通过降低中枢神经系统中的 Th1 样、Th17 和 TNF-α 细胞因子并增加中枢神经系统中的 Th2 样细胞因子 (IL-13) 来抑制中枢神经系统炎症。
