NHC Key Laboratory of Biotechnology of Antibiotics, CAMS Key Laboratory of Synthetic Biology for Drug Innovation, Institute of Medicinal Biotechnology, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
Inner Mongolia Medical University, Inner Mongolia People's Hospital, Hohhot, China.
Front Immunol. 2021 Apr 26;12:662362. doi: 10.3389/fimmu.2021.662362. eCollection 2021.
Psoriasis is a recurrent autoimmune skin disease with aberrant regulation of keratinocytes and immunocytes. There is no universally accepted single treatment available for psoriasis, and the establishment of a common treatment option to control its signs and symptoms is urgently needed. Here, we found Ebosin, a novel exopolysaccharide isolated from sp. 139 by our lab, not only could ameliorate inflammation in LPS-induced keratinocytes through IKK/NF-kapaB pathway, but also attenuate psoriatic skin lesions and reduce inflammatory factors expression in imiquimod (IMQ)-mediated psoriatic mice. Except for inhibiting the expression of epidermal differentiation related proteins, Ebosin significantly increased the percentage of CD4Foxp3CD25 Tregs and decreased CD4IL17A Th17 cells in psoriatic mice. Furthermore, we demonstrate that Ebosin significantly suppressed the IL-17 signaling pathway A20 (encoded by ) . As the direct binding of to miR-155 has been demonstrated by luciferase reporter assay, and Ebosin has been demonstrated to inhibit miR-155 level and , our study first indicates that Ebosin reduces inflammation through the miR-155--IL-17 axis and T cell differentiation in a psoriasis-like model. Thus, we conclude that Ebosin can act as a promising therapeutic candidate for the treatment of psoriasis.
银屑病是一种复发性自身免疫性皮肤病,其角质形成细胞和免疫细胞的调节异常。目前尚无普遍接受的单一治疗方法可用于银屑病,迫切需要建立一种共同的治疗选择来控制其症状和体征。在这里,我们发现了一种新型胞外多糖 Ebosin,它是由我们实验室从 sp. 139 中分离得到的。Ebosin 不仅可以通过 IKK/NF-kapaB 途径改善 LPS 诱导的角质形成细胞中的炎症,还可以减轻银屑病小鼠的皮肤损伤并降低咪喹莫特 (IMQ) 介导的银屑病小鼠中的炎症因子表达。除了抑制表皮分化相关蛋白的表达外,Ebosin 还显著增加了银屑病小鼠中 CD4Foxp3CD25 Treg 的比例,并减少了 CD4IL17A Th17 细胞。此外,我们证明 Ebosin 显著抑制了 IL-17 信号通路 A20(由 编码)。由于已通过荧光素酶报告基因检测证实了 与 miR-155 的直接结合,并且 Ebosin 已被证明可以抑制 miR-155 的水平 和 ,我们的研究首次表明 Ebosin 通过 miR-155--IL-17 轴和 T 细胞分化在银屑病样模型中减轻炎症。因此,我们得出结论,Ebosin 可以作为治疗银屑病的有前途的治疗候选物。