Calabrese Francesca, Rossetti Andrea C, Racagni Giorgio, Gass Peter, Riva Marco A, Molteni Raffaella
Department of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano Milan, Italy.
Department of Psychiatry and Psychotherapy, Research Group Animal Models in Psychiatry, Central Institute of Mental Health, Medical Faculty Mannheim/Heidelberg University Mannheim, Germany.
Front Cell Neurosci. 2014 Dec 22;8:430. doi: 10.3389/fncel.2014.00430. eCollection 2014.
Cytokines are key regulatory mediators involved in the host response to immunological challenges, but also play a critical role in the communication between the immune and the central nervous system. For this, their expression in both systems is under a tight regulatory control. However, pathological conditions may lead to an overproduction of pro-inflammatory cytokines that may have a detrimental impact on central nervous system. In particular, they may damage neuronal structure and function leading to deficits of neuroplasticity, the ability of nervous system to perceive, respond and adapt to external or internal stimuli. In search of the mechanisms by which pro-inflammatory cytokines may affect this crucial brain capability, we will discuss one of the most interesting hypotheses: the involvement of the neurotrophin brain-derived neurotrophic factor (BDNF), which represents one of the major mediators of neuroplasticity.
细胞因子是参与宿主对免疫挑战反应的关键调节介质,同时在免疫和中枢神经系统之间的通信中也起着关键作用。因此,它们在这两个系统中的表达受到严格的调控。然而,病理状况可能导致促炎细胞因子的过度产生,这可能对中枢神经系统产生有害影响。特别是,它们可能损害神经元结构和功能,导致神经可塑性(即神经系统感知、响应和适应外部或内部刺激的能力)缺陷。为了探寻促炎细胞因子可能影响这种关键脑功能的机制,我们将讨论一个最有趣的假说:神经营养因子脑源性神经营养因子(BDNF)的参与,它是神经可塑性的主要介质之一。