感染是创伤性脑损伤 (TBI) 后最常见的并发症之一，目前多数研究都局限于感染发生的外因方面，注重感染的危险因素，而从内因方面进行探讨相对空白。我们前期临床研究表明TBI患者伴有交感神经活性的升高及细胞免疫功能的抑制，这在合并感染的患者中尤为显著。因此，本研究首先建立TBI大鼠模型，观察其交感活性、单核细胞β2-肾上腺素受体(AR)/NF-κB/HLA-DR通路活性及细胞免疫状态，及阻滞该通路对细胞免疫功能的影响。其次，以交感活性物质体外干预THP-1单核细胞株，并给予通路阻滞剂处理，观察其免疫活性状态的改变。第三，动态检测TBI患者的交感活性、单核细胞β2-AR/NF-κB/HLA-DR通路活性及细胞免疫功能。本研究旨在从动物、细胞及临床三个层面研究TBI后交感神经激活对单核细胞β2-AR/NF-κB/HLA-DR通路及免疫功能的影响，明确其在感染发生中所扮演的角色及相应机制。

As a leading cause of death and the most common complication following traumatic brain injury (TBI), infection has received considerable attention in the clinical practice. Unfortunately, although intensive researches have been carried out in this area, the therapeutic interventions remain limited. Current studies are mainly focused on searching the risk factors for infection and controlling these risk factors in order to reduce the incidence of infection. However, to date, it is little known about the role of cross-talk between the nervous system and the immune system in the development of infection after TBI. Our previous clinical study has shown that there is significant sympathetic activation and inhibition of cellular immune response following TBI, especially in the one with infection. In the present study, research strategies are as followed. Firstly, in in vivo study, TBI is induced in rats using the modified Feeney’s weight-drop model. The activity of sympathetic nervous system, the β2-adrenoceptor(AR)/NF-κB/HLA-DR pathway of the monocytes, and the immune function are evaluated in the TBI rats with or without the pathway blockade by investigating the expression of peripheral blood-based markers such as metanephrine (MN), normetanephrine (NMN), interferon-γ (IFN-γ), interleukin-10 (IL-10), class II major histocompatibility complex (MHC II), CD86 and CII TA. Secondly, in in vitro study, MN and NMN are administered in the monocytic cell lines such as the THP-1 cell line to mimic sympathetic activation. The expressions of NF-κB, MHC II, CD86 and CII TA in the THP-1 cell line are examined to show the immune function in the monocytes with or without the treatment with the blockade of β2-AR/NF-κB/HLA-DR pathway. Thirdly, the peripheral blood in the patients with TBI is collected to dynamically investigate the activity of sympathetic nervous system, the β2-AR/NF-κB/HLA-DR pathway of the monocytes, and the immune function. Overall, our study is aimed to investigate the effects of TBI-induced sympathetic activation on the monocytic β2-AR/NF-κB/HLA-DR pathway and immune function from bench to bedside. The anticipated results of the present study will be beneficial to reveal the role of sympathetic activation in the incidence of infection, which can promote the clinical application of sympathetic block and provide theoretical support for the clinical application in the patients with TBI.