van Duinen Marlies A, Schruers Koen R J, Kenis Gunter R L, Wauters Annick, Delanghe Joris, Griez Eric J L, Maes Michael H J
School of Mental Health and Neurosciences, Maastricht University, The Netherlands.
J Psychosom Res. 2008 Mar;64(3):305-10. doi: 10.1016/j.jpsychores.2007.10.004.
Psychoimmunological research in panic disorder (PD) so far focussed on single time point evaluation in resting conditions. No robust evidence for changes in the immune system was found using this method. However, PD is characterized by the occurrence of unexpected panic attacks (PAs). The current research focuses on cytokine and acute phase protein (APP) levels and mitogen-induced cytokine secretion following 35% CO(2) inhalation-induced panic.
Eighteen PD patients and 18 matched healthy control subjects underwent both a placebo and a 35% CO(2) inhalation on separate days. Blood samples for cytokine and APP determination were taken before and after the inhalation. In addition to serum determination, whole blood samples were cultured and stimulated with mitogens for assessment of the functional capacity of the immune system.
The 35% CO(2) inhalation induced significantly higher levels of anxiety in PD patients as compared to the control subjects, but no differences in immune parameters were found, either in basal conditions or after experimental panic induction.
In our sample we do not find any changes in serum levels or functional capacity of several immunological parameters in the experimentally provoked PAs. Similar results have been found in social phobia, whereas in other affective disorders such as depression and posttraumatic stress disorder, immune changes are evident. Changes seem to coincide with alterations in hypothalamic-pituitary-adrenal (HPA) axis function. Therefore, the bidirectional communication pathway between the immune system and the HPA axis might play a role in some affective disorders, but it does not specifically seem to be involved in the etiology of PD.
迄今为止，惊恐障碍（PD）的心理免疫学研究主要集中在静息状态下的单次时间点评估。使用这种方法未发现免疫系统变化的确凿证据。然而，PD的特征是意外惊恐发作（PA）的出现。当前的研究聚焦于35%二氧化碳吸入诱发惊恐后细胞因子和急性期蛋白（APP）水平以及丝裂原诱导的细胞因子分泌。
18名PD患者和18名匹配的健康对照受试者在不同日期分别接受安慰剂和35%二氧化碳吸入。在吸入前后采集用于测定细胞因子和APP的血样。除了血清测定外，还对全血样本进行培养并用丝裂原刺激，以评估免疫系统的功能能力。
与对照受试者相比，35%二氧化碳吸入使PD患者的焦虑水平显著更高，但在基础状态或实验性惊恐诱发后，未发现免疫参数有差异。
在我们的样本中，我们未发现实验诱发的惊恐发作中几种免疫参数的血清水平或功能能力有任何变化。在社交恐惧症中也发现了类似结果，而在其他情感障碍如抑郁症和创伤后应激障碍中，免疫变化是明显的。这些变化似乎与下丘脑 - 垂体 - 肾上腺（HPA）轴功能的改变相吻合。因此，免疫系统与HPA轴之间的双向通信通路可能在某些情感障碍中起作用，但似乎并不特别涉及PD的病因。
