Division of Oral Biology, College of Dentistry, The Ohio State University, Columbus, OH, USA.
Brain Behav Immun. 2013 Mar;30 Suppl:S41-7. doi: 10.1016/j.bbi.2012.06.015. Epub 2012 Jul 9.
Stress-induced immune dysregulation results in significant health consequences for immune related disorders including viral infections, chronic autoimmune disease, and tumor growth and metastasis. In this mini-review we discuss the sympathetic, neuroendocrine and immunologic mechanisms by which psychosocial stress can impact cancer biology. Both human and animal studies have shown the sympathetic and neuroendocrine responses to psychosocial stress significantly impacts cancer, in part, through regulation of inflammatory mediators. Psychosocial stressors stimulate neuroendocrine, sympathetic, and immune responses that result in the activation of the hypothalamic-pituitary-adrenal (HPA)-axis, sympathetic nervous system (SNS), and the subsequent regulation of inflammatory responses by immune cells. Social disruption (SDR) stress, a murine model of psychosocial stress and repeated social defeat, provides a novel and powerful tool to probe the mechanisms leading to stress-induced alterations in inflammation, tumor growth, progression, and metastasis. In this review, we will focus on SDR as an important model of psychosocial stress in understanding neural-immune mechanisms in cancer.
应激引起的免疫失调可导致包括病毒感染、慢性自身免疫性疾病以及肿瘤生长和转移等与免疫相关的疾病产生严重后果。在本篇综述中，我们讨论了心理社会压力影响癌症生物学的交感神经、神经内分泌和免疫机制。人类和动物研究均表明，心理社会压力的交感神经和神经内分泌反应显著影响癌症，部分原因是通过调节炎症介质。心理社会应激源刺激神经内分泌、交感神经和免疫反应，导致下丘脑-垂体-肾上腺（HPA）轴、交感神经系统（SNS）的激活，以及随后免疫细胞对炎症反应的调节。社会剥夺（SDR）应激是一种心理社会应激和反复社会挫败的小鼠模型，为探究导致应激引起的炎症、肿瘤生长、进展和转移改变的机制提供了一种新的有力工具。在这篇综述中，我们将重点关注 SDR 作为理解癌症中神经免疫机制的重要心理社会压力模型。
