译作分享
炎症:与压力有关的疾病的共同途径
上期回顾
接上文
Stress, Inflammation and Depression
压力、炎症和抑郁症
Stressful experiences are fundamental in the provocation of major depression of disorder (MDD). HPA axis activation and hypercortisolemia often seen in depressed patients may represent increased stress hormones, CRH and ACTH secretion (Capuron et al., 2003). MAPK pathways have been proved to increase the activity of serotonin membrane transporters, the most important neurotransmitter associated with depression (Zhu et al., 2006).
压力的经历是诱发重度抑郁症(MDD)的根本原因。在抑郁症患者中经常看到HPA轴激活和高皮质醇血症,可能代表应激激素、CRH和ACTH分泌的增加 (Capuron et al., 2003))。MAPK通路已被证明可以增加血清素膜转运蛋白的活性,而血清素膜转运蛋白是与抑郁症相关的最重要的神经递质 (Zhu et al., 2006)。
Stress, Inflammation and
Neurodegenerative Diseases
压力、炎症和神经退行性疾病
The role of stress and inflammation are being recognized in neurodegenerative disease. AD and PD are the two most common neurodegenerative diseases. Extracellular amyloid β protein (Aβ) accumulation is currently seen as a key step in the pathogenesis of AD. PD is characterized by progressive loss of nigrostriatal dopaminergic (DA) neurons and depletion of dopamine in the striatum, which lead to pathological and clinical abnormalities. The potential etiology and molecular mechanisms underlying the pathogenesis of AD and PD remains unknown and have not been completely elucidated. However, some progress has been made in identifying the risk factors. During the last two to three decades, increasing evidence from animal and clinical studies has implicated stress and neuroinflammation as risk factors and may play a fundamental part in the pathogenesis of AD and PD.
Epidemiological, clinical studies and animal model of AD suggest that stress and inflammation interact with processing and deposit of Aβ, contributing to the pathogenesis of AD (Kunjathoor et al., 2004). Hypercortisolemia is one of the features found in patients diagnosed of AD. An array of elevated inflammatory mediators including TNFα, IL-1, PGE2, NF-κB, COX-2 and MCP-1 has been detected from patients with AD (Wyss-Coray, 2006; Comi et al., 2010) and correlated with the amount of Aβ and the severity of AD pathogenesis (Hoshino et al., 2009; Chen et al., 2012). Researchers also observed increased cytokines such as TNFα, IL-1β and IFN in the substantianigra of PD patients (Nagatsu and Sawada, 2005). Activation of the systemic innate immune system by infection may participate in the early stages of AD pathogenesis (Perry et al., 2007). Neuroinflammation induces degenerative changes in the DA system, which lowers the set point toward neuronal dysfunction and degeneration (Morand and Leech, 1999). Proinflammatory lipid mediators include PGs and platelet activating factor, together with cytokines may significantly affect the progressive neurodegeneration in PD (Busillo et al., 2011). Mice with microglial activation-induced oxidative stress and inflammation, and nigrostriatal DA neuronal damage have been used to serve as an experimental model of PD. Stress exposure increased neuroinflammation in AD and is characterized by astrogliosis, increased inflammatory gene expression and lipid peroxidation (Perez Nievas et al., 2011). It has been confirmed with the changes in glial cells surrounding the senile plaques. Genetic research demonstrates that inherited variations in inflammatory response mechanisms may influence AD pathogenesis (Grimaldi et al., 2000; Nicoll et al., 2000). In contrast, anti-inflammatory agents such as NSAIDs and antioxidant therapy might protect against the development of AD. Long-term use of NSAIDs, inhibitors of COX, suppression of neuroinflammation by glial inhibitors, delays the initiation and reduces the risk of AD (Tsukuda et al., 2009; Chen et al., 2012). In consistent with epidemiology, nicotine was proved to have a neuroprotective effect on DA neurons by means of an anti-inflammatory mechanism mediated by the regulation of microglial activation (Park et al., 2007). Therefore, new potent neuroprotective therapies for PD might be taken into account by focusing on critical inflammatory mechanisms, such as cytokine-induced neurotoxicity (Morand and Leech, 1999). A variety of preclinical studies have corroborated the therapeutic potential of targeting cholinergic anti-inflammatory pathway (Bencherif et al., 2011).
AD的流行病学、临床研究和动物模型表明,压力和炎症与Aβ的处理和沉积相互作用,促进了AD的发病机制 (Kunjathoor et al., 2004)。高皮质醇血症是在被诊断为AD的患者中发现的特征之一。从AD患者中检测到一系列升高的炎症介质,包括TNFα,IL-1,PGE2,NF-κB,COX-2和MCP-1 (Wyss-Coray, 2006; Comi et al., 2010) 并与Aβ的量和AD发病机制的严重程度相关 (Hoshino et al., 2009; Chen et al., 2012)。研究人员还观察到PD患者的下丘脑中的TNFα,IL-1β和IFN等细胞因子增加 (Nagatsu and Sawada, 2005)。感染对全身先天免疫系统的激活可能参与了AD发病机制的早期阶段 (Perry et al., 2007)。神经炎症诱导DA系统中的退行性变化,从而降低神经元功能障碍和变性的设定点 (Morand and Leech, 1999)。促炎性脂质介质包括PGs和血小板激活因子,以及细胞因子可能显着影响PD的进行性神经退化 (Busillo et al., 2011)。具有小胶质细胞激活诱导的氧化应激和炎症以及黑纹状体DA神经元损伤的小鼠已被用作PD的实验模型。压力暴露增加了AD中的神经炎症,其特征在于星形胶质细胞增多,炎症基因表达增加和脂质过氧化增加 (Perez Nievas et al., 2011)。老年斑块周围神经胶质细胞的变化证实了这一点。遗传研究表明,炎症反应机制的遗传变异可能会影响AD发病机制 (Grimaldi et al., 2000; Nicoll et al., 2000)。相反,抗炎剂如NSAIDs和抗氧化剂疗法可以防止AD的发展。 长期使用NSAIDs,COX抑制剂,通过神经胶质抑制剂抑制神经炎症,可延AD的发生并降低其风险 (Tsukuda et al., 2009; Chen et al., 2012)。与流行病学一致,尼古丁被证明通过由小胶质细胞激活调节介导的抗炎机制对DA神经元具有神经保护作用 (Park et al., 2007)。因此,可以通过关注关键的炎症机制来考虑PD的新的有效神经保护疗法,例如细胞因子诱导的神经毒性 (Morand and Leech, 1999)。各种临床前研究证实了靶向胆碱能抗炎途径的治疗潜力(Bencherif et al., 2011)。
Stress, Inflammation and Cancer
压力、炎症和癌症
经典的应激信号,β肾上腺素能信号激活被认为是胰腺癌、急性淋巴细胞白血病、乳腺癌进展和侵袭的主要原因(Lamkin et al., 2012; Kim-Fuchs et al., 2014; Qin et al., 2015)。这些效应被证明与肿瘤细胞中侵袭基因表达的增加有关。 药理学β肾上腺素能阻断拮抗剂可以逆转观察到的慢性应激对癌症进展的影响。 此外,通过βAR激动剂激活β肾上腺素能信号,可以降低高度转移的人乳腺癌细胞、卵巢、前列腺、黑色素瘤和白血病细胞的变形性,这取决于肌动蛋白细胞骨架和肌球蛋白II的活性。细胞变形性的这些变化可以通过药物β阻断或β2-肾上腺素能受体(β2-AR) (Kim et al., 2016)。除βAR外,儿茶酚胺也向α肾上腺素能受体发出信号。相反,α2-肾上腺素能信号传导被证明可以通过自身感受器机制抑制交感神经儿茶酚胺的释放。选择性α2-肾上腺素能阻断模拟慢性压力对乳腺癌进展的加速作用 (Lamkin et al., 2015)。
The β2-ARs are expressed on multiple cell types involved in immunoregulation, including not only immune cells (Theron et al., 2013; Padro and Sanders, 2014), but also non-immune cells with a bystander role in the immune response (e.g., glia cells, fibroblasts, endothelial cells, etc.; Mantyh et al., 1995; Johnson, 2006). Stress-induced epinephrine binds to β2-ARs, and then results in the activation of p38 MAPK, which in turn enhances NF-κB DNA binding and cytokines and chemokines expression (Kolmus et al., 2015). More recently, stress-mediated immune modulation of cytokines including TNF-α, TGF-β, IL-1 and IL-6 have been suggested as indictors of cancer progression, metastasis and recurrence. Additionally, in some cancers (e.g., colon, renal cell, lung and breast) secretion of these same cytokines by tumor cells helps drive and sustain pro-tumorigenic inflammatory loops (Angelo et al., 2002; Gao et al., 2007). Among several cytokines, IL-6 is the most studied pro-inflammatory factor in tumor. Circulating levels of IL-6 have been reported as forecast cytokine of survival and metastasis in human cancers (Chung and Chang, 2003; Salgado et al., 2003; Pierce et al., 2009). Several studies revealed that high serum concentration of IL-6 is a prognostic indicator of poor outcome in cancer patients with diverse tumor types including gastric, pancreatic, melanoma, breast, colorectal, myeloma and lung cancer (Heikkilä et al., 2008; Lippitz, 2013). A higher lung cancer risk for participants with elevated concentrations of IL-6 was observed in recent clinical trial (Brenner et al., 2017). In animal studies, IL-6 trans-signaling is linked to tumor development in inflammation-induced colorectal and pancreatic cancer (Grivennikov et al., 2009; Rose-John, 2012). Moreover, evidence that disruption of IL-6 trans-signaling delays growth in established murine tumors demonstrates that IL-6 activities are important during neoplastic progression (Grivennikov et al., 2009; Rose-John, 2012). IL-6 trans-signaling-dependent activation of STAT3 can drive cancer progression through the transcription of target genes including the cell cycle regulator cyclin D1, the proto-oncogene c-myc, transcriptional regulators such as JunB, cFos, C/EBPβ and C/EBPδ, and metabolic regulators such as mTORC1 (Hirano et al., 2000; Thiem et al., 2013). IL-6 blockade would change immunological environment and reinforce the effectiveness of anti-programmed death-1-ligand 1 (anti-PD-L1) therapy, therefore evoking significant tumor suppression activity in pancreatic ductal adenocarcinoma (Mace et al., 2016); additionally, neutralization of IL-6 abrogated hepatocellular carcinoma (HCC) progression and myeloid-derived suppressive cells (MDSC) accumulation in Rarres2−/− mice (Lin et al., 2017). Taken together, evidence linking stress to cancer progression and inflammation provide penetration into the magnitude of modulation of cancer-related cytokines (e.g., IL-6) that appear to alleviate the effects of stress on cancer.
Conclusion
结论
总结,通过扰乱免疫系统的平衡,压力会诱发外周和中枢炎症。这种不平衡导致了多种与压力相关的疾病。虽然可能有各种不同的触发事件,但它们似乎都收敛于炎症。在这篇综述文章中,我们提供了证据表明压力通过外周炎症和神经炎症诱发或恶化心血管疾病、非酒精性脂肪肝、抑郁症、神经退行性疾病和癌症。压力主要通过激活SNS和HPA轴而使中枢小胶质细胞和星形胶质细胞、血管、免疫系统和肝脏参与进来(图1A)。 因此,我们认为炎症可能是与压力相关疾病的共同途径,它可能是导致疾病进展的一个因素,也可能在疾病发展的早期发生。图1B显示,包括遗传易感性、衰老和生活方式在内多因素因子,作用于与压力相关的疾病,而压力诱发的慢性低度炎症也是多种慢性病的共同土壤。
FIGURE 1/图1
Limitations
限制条件
Stress-induced inflammation described here may be relevant to understand the common mechanisms of stress-related diseases. However, quite a few unanswered questions still need to be further discussed. For instance, besides inflammation, is there the crosstalk among inflammation and other related pathways such as cell stress? Is there the specific cell or pathway for the specific stress-related disease? Can anti-inflammatory specifically affect neuroinflammation without modulating periphery immunity for CNS disease? More crucially, to reach clinical application, anti-inflammatory therapies will need to accurately target on specific cells and pathways in CNS, which are fundamentally important in human disease pathogenesis. All these limitations could be the next research key point. Breaking through these barriers would make great progress on the treatment of stress-related diseases.
Future Directions
未来方向
Author Contribution
作者的贡献
Conflict of Interest Statement
利益冲突声明
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Acknowledgements
鸣谢
THE END
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