Nettleford Shaneice K, Prabhu K Sandeep
Center for Molecular Immunology and Infectious Disease and Center for Molecular Toxicology and Carcinogenesis, The Pennsylvania State University, University Park, PA 16802, USA.
Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, University Park, PA 16802, USA.
Antioxidants (Basel). 2018 Mar 1;7(3):36. doi: 10.3390/antiox7030036.
Inflammatory bowel disease (IBD), characterized by severe flares and remissions, is a debilitating condition. While the etiology is unknown, many immune cells, such as macrophages, T cells and innate lymphoid cells, are implicated in the pathogenesis of the disease. Previous studies have shown the ability of micronutrient selenium (Se) and selenoproteins to impact inflammatory signaling pathways implicated in the pathogenesis of the disease. In particular, two transcription factors, nuclear factor-κB (NF-κB), and peroxisome proliferator activated receptor (PPAR)γ, which are involved in the activation of immune cells, and are also implicated in various stages of inflammation and resolution, respectively, are impacted by Se status. Available therapies for IBD produce detrimental side effects, resulting in the need for alternative therapies. Here, we review the current understanding of the role of NF-κB and PPARγ in the activation of immune cells during IBD, and how Se and selenoproteins modulate effective resolution of inflammation to be considered as a promising alternative to treat IBD.
炎症性肠病（IBD）以严重发作和缓解为特征，是一种使人衰弱的疾病。虽然其病因尚不清楚，但许多免疫细胞，如巨噬细胞、T细胞和固有淋巴细胞，都与该疾病的发病机制有关。先前的研究表明，微量营养素硒（Se）和硒蛋白能够影响与该疾病发病机制相关的炎症信号通路。特别是，两种转录因子，即参与免疫细胞激活的核因子-κB（NF-κB）和过氧化物酶体增殖物激活受体（PPAR）γ，分别在炎症的各个阶段和炎症消退过程中发挥作用，它们会受到硒状态的影响。IBD的现有疗法会产生有害的副作用，因此需要替代疗法。在此，我们综述了目前对NF-κB和PPARγ在IBD期间免疫细胞激活中的作用的理解，以及硒和硒蛋白如何调节炎症的有效消退，从而有望成为治疗IBD的替代方法。
