State Key Laboratory of Trauma, Burns and Combined Injury, Institute of Surgery Research, Daping Hospital, Third Military Medical University, Chongqing, 400042, China.
Int J Biol Sci. 2017 Nov 1;13(11):1409-1419. doi: 10.7150/ijbs.21916. eCollection 2017.
During the occurrence and development of injury (trauma, hemorrhagic shock, ischemia and hypoxia), the neuroendocrine and immune system act as a prominent navigation leader and possess an inter-system crosstalk between the reciprocal information dissemination. The fundamental reason that neuroendocrinology and immunology could mix each other and permeate toward the field of traumatology is owing to their same biological languages or chemical information molecules (hormones, neurotransmitters, neuropeptides, cytokines and their corresponding receptors) shared by the neuroendocrine and immune systems. The immune system is not only modulated by the neuroendocrine system, but also can modulate the biological functions of the neuroendocrine system. The interactive linkage of these three systems precipitates the complicated space-time patterns for the courses of traumatic inflammation. Recently, compelling evidence indicates that the network linkage pattern that initiating agents of neuroendocrine responses, regulatory elements of immune cells and effecter targets for immune regulatory molecules arouse the resistance mechanism disorders, which supplies the beneficial enlightenment for the diagnosis and therapy of traumatic complications from the view of translational medicine. Here we review the alternative protective and detrimental roles as well as possible mechanisms of the neuroendocrine immune responses in traumatic inflammation.
在损伤（创伤、失血性休克、缺血缺氧）发生和发展过程中，神经内分泌系统和免疫系统作为突出的导航领导者，具有相互信息传递的系统间串扰。神经内分泌学和免疫学能够相互混合并渗透到创伤学领域的根本原因是它们具有相同的生物语言或化学信息分子（激素、神经递质、神经肽、细胞因子及其相应的受体），这些分子由神经内分泌系统和免疫系统共享。免疫系统不仅受到神经内分泌系统的调节，还可以调节神经内分泌系统的生物学功能。这三个系统的相互联系导致了创伤性炎症过程中复杂的时空模式。最近，有强有力的证据表明，神经内分泌反应的启动剂、免疫细胞的调节因子和免疫调节分子的效应靶点之间的网络联系模式引起了抵抗机制的紊乱，这从转化医学的角度为创伤性并发症的诊断和治疗提供了有益的启示。在这里，我们回顾了神经内分泌免疫反应在创伤性炎症中的替代保护和有害作用及其可能的机制。
