Molecular Immunopharmacology and Drug Discovery Laboratory, Department of Molecular Physiology and Pharmacology, Tufts University School of Medicine, Boston, MA 02111, USA.
Autoimmun Rev. 2013 Aug;12(10):947-53. doi: 10.1016/j.autrev.2013.02.006. Epub 2013 Mar 26.
Substantial evidence indicates that stress can precipitate or worsen symptoms of inflammation in general and more specifically in multiple sclerosis (MS), a demyelinating, autoimmune disease characterized by inflammation of the central nervous system (CNS). However, the mechanism of how stress affects MS is not well understood. We reviewed publications in PubMed since 1995 and propose that neuropeptides secreted under stress, such as corticotropin releasing hormone (CRH) and neurotensin (NT), activate microglia and mast cells to release inflammatory molecules. These lead to maturation and activation of T17 autoimmune cells, disruption of the blood-brain barrier (BBB) and T cell entry into the CNS, thus promoting brain inflammation and contributing to MS pathology. Reduction of stress and inhibition of these processes by select flavonoids could provide novel therapeutic approaches.
大量证据表明,压力可引发或加重炎症的症状,一般而言,也可加重多发性硬化症(MS)的症状,MS 是一种脱髓鞘自身免疫性疾病,其特征是中枢神经系统(CNS)炎症。然而,压力影响 MS 的机制尚不清楚。我们回顾了自 1995 年以来在 PubMed 上发表的出版物,并提出在压力下分泌的神经肽,如促肾上腺皮质激素释放激素(CRH)和神经降压素(NT),可激活小胶质细胞和肥大细胞释放炎症分子。这些炎症分子导致 T17 自身免疫细胞的成熟和激活、血脑屏障(BBB)的破坏以及 T 细胞进入中枢神经系统,从而促进大脑炎症并导致 MS 病理。通过选择类黄酮减少压力和抑制这些过程可能提供新的治疗方法。