Dragoş Dorin, Tănăsescu Maria Daniela
Carol Davila University of Medicine and Pharmacy Bucharest, Romania.
J Med Life. 2010 Jan-Mar;3(1):10-8.
Acute stress increases resistance to infection. The alteration of this mechanism in chronically stressed people impairs the organism's ability to mount a strong immune response with a resultant increase in morbidity. Acute stress induces a probable sympatho-adrenergically mediated increase in chemotaxis and adhesion molecules expression, thus promoting immune cells migration to sites of infection and/or inflammation, while chronic stress impairs this mechanism. Protracted stressful conditions decrease NK cytotoxic capacity. There is a substance P, which under stressful circumstances mediates the increase in macrophage cytokine production. Acute stress increases T cell mobilization through a beta2-adrenergically mediated process, which is blunted during chronic stress. Psychological stress impairs the immune system's ability to produce antibodies in response to a vaccine, thereby making the organism more vulnerable to infections.
急性应激会增强抗感染能力。长期处于应激状态的人，这种机制发生改变，会损害机体产生强烈免疫反应的能力，进而导致发病率增加。急性应激可能通过交感 - 肾上腺素能介导，使趋化性和黏附分子表达增加，从而促进免疫细胞迁移至感染和/或炎症部位，而慢性应激则会损害这一机制。长期的应激状态会降低自然杀伤细胞的细胞毒性能力。有一种P物质，在应激情况下可介导巨噬细胞细胞因子产生增加。急性应激通过β2 - 肾上腺素能介导的过程增加T细胞动员，而在慢性应激期间这一过程会减弱。心理应激会损害免疫系统对疫苗产生抗体的能力，从而使机体更容易受到感染。
