Dantzer R
INRA-INSERM U394, Bordeaux Cedex, 33077, France.
Brain Behav Immun. 2001 Mar;15(1):7-24. doi: 10.1006/brbi.2000.0613.
Sickness behavior refers to the coordinated set of behavioral changes that develop in sick individuals during the course of an infection. At the molecular level, these changes are due to the effects of proinflammatory cytokines, such as interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNFalpha), in the brain. Peripherally released cytokines act on the brain via a fast transmission pathway involving primary afferent nerves innervating the body site of inflammation and a slow transmission pathway involving cytokines originating from the choroid plexus and circumventricular organs and diffusing into the brain parenchyma by volume transmission. At the behavioral level, sickness behavior appears to be the expression of a central motivational state that reorganizes the organism's priorities to cope with infectious pathogens. There is clinical and experimental evidence that activation of the brain cytokine system is associated with depression, although the exact relationship between sickness behavior and depression is still elusive.
疾病行为是指患病个体在感染过程中发生的一系列协调性行为变化。在分子水平上，这些变化是由促炎细胞因子，如白细胞介素-1（IL-1）和肿瘤坏死因子-α（TNFα）在大脑中的作用引起的。外周释放的细胞因子通过一条快速传递途径作用于大脑，该途径涉及支配炎症身体部位的初级传入神经，以及一条缓慢传递途径，该途径涉及源自脉络丛和室周器官的细胞因子，并通过容积传递扩散到脑实质中。在行为水平上，疾病行为似乎是一种中枢动机状态的表现，这种状态会重新组织机体的优先事项以应对感染性病原体。有临床和实验证据表明，大脑细胞因子系统的激活与抑郁症有关，尽管疾病行为与抑郁症的确切关系仍不清楚。
