Rheumatology Research Group, School of Immunity and Infection, College of Medical and Dental Sciences, University of Birmingham, United Kingdom.
Swiss Med Wkly. 2013 Jan 21;143:w13743. doi: 10.4414/smw.2013.13743. eCollection 2013.
Inflammation is an important component of normal responses to infection and injury. However, chronic activation of the immune system, due to aberrant responses to normal stimuli, can lead to the establishment of a persistent inflammatory state. Such inflammatory conditions are often debilitating, and are associated with a number of important co-morbidities including cardiovascular disease. Resting non-proliferative tissues have distinctive metabolic activities and requirements, which differ considerably from those in infiltrating immune cells, which are undergoing proliferation and differentiation. Immune responses in tissues may therefore be modulated by the relative abundance of substrates in the inflamed site. In turn immune cell activity can feed back and affect metabolic behaviour of the tissues, as most clearly demonstrated in cachexia - the loss of cellular mass driven by tumour necrosis factor-alpha (TNF-α) a key mediator of the inflammatory response. Here we discuss the potential for metabolomic analysis to clarify the interactions between inflammation and metabolic changes underlying many diseases. We suggest that an increased understanding of the interaction between inflammation and cellular metabolism, energy substrate use, tissue breakdown markers, the microbiome and drug metabolites, may provide novel insight into the regulation of inflammatory diseases.
炎症是对感染和损伤的正常反应的重要组成部分。然而，由于对正常刺激的异常反应，免疫系统的慢性激活可能导致持续的炎症状态的建立。这种炎症状态通常使人虚弱，并与许多重要的合并症相关，包括心血管疾病。静止的非增殖组织具有独特的代谢活性和需求，与浸润免疫细胞的代谢活性和需求有很大的不同，浸润免疫细胞正在增殖和分化。因此，组织中的免疫反应可能受到炎症部位中底物相对丰度的调节。反过来，免疫细胞的活性可以反馈并影响组织的代谢行为，这在肿瘤坏死因子-α（TNF-α）驱动的恶病质中最为明显，TNF-α 是炎症反应的关键介质。在这里，我们讨论了代谢组学分析在阐明许多疾病的炎症和代谢变化之间相互作用的潜力。我们认为，增加对炎症与细胞代谢、能量底物利用、组织分解标志物、微生物组和药物代谢物之间相互作用的理解，可能为炎症性疾病的调控提供新的见解。
