Abstract—The aim of the study was to identify changes in serum concentrations of pro- and anti-inflammatory cytokines in workers exposed to metallic mercury vapors and in patients with chronic mercury intoxication (CMI), depending on the level of depression. We found unidirectional changes in the cytokine profile in workers with moderate and severe depression chronically exposed to vapors of metallic mercury, which include an increase in the production of proinflammatory IL-6 and TNF-α, and a decrease in IL-2. The most pronounced activity of inflammatory reactions was observed in subjects with moderate depression. In patients with severe depression associated with CMI, we found IL-4 overproduction associated with a decrease in the activation of pro-inflammatory reactions (IL-6, TNF-α) and an increase in IL-2 concentrations relative to subjects with moderate depression, which may reflect disturbance of the adequate functioning of the mechanisms cytokine regulation of the immune response. The revealed changes in the cytokine profile may be due to the comorbidity of depression with organic disorders of the nervous system characteristic of CMI, which can alter the state of the immune system. Further analysis of the role of inflammatory mediators in the pathophysiological mechanisms of the formation and development of depressive disorders will make it possible to more accurately determine objective risk criteria and develop preventive measures that will help to reduce the contribution of depression to the overall picture of neurointoxication.

摘要这项研究的目的是根据抑郁症的程度，确定暴露于金属汞蒸气的工人和患有慢性汞中毒（CMI）的患者血清中促炎和抗炎细胞因子的浓度变化。我们发现长期暴露于金属汞蒸气的中度和重度抑郁工人的细胞因子谱具有单向变化，包括促炎性IL-6和TNF-α的产生增加以及IL-2的减少。在中度抑郁的受试者中观察到最明显的炎症反应活性。在伴有CMI的严重抑郁症患者中，我们发现IL-4过度生产与促炎性反应的激活减少有关（IL-6，相对于中度抑郁的受试者，TNF-α）和IL-2浓度增加，这可能反映出细胞因子调节免疫应答机制的充分功能受到干扰。细胞因子特征的显着变化可能是由于抑郁症与CMI特征的神经系统器质性疾病合并症所致，它可以改变免疫系统的状态。炎性介质在抑郁症形成和发展的病理生理机制中的作用的进一步分析将使更准确地确定客观风险标准和制定预防措施成为可能，这将有助于减少抑郁症对神经中毒总体状况的影响。这可能反映了对免疫应答的细胞因子调节机制的适当功能的干扰。细胞因子特征的显着变化可能是由于抑郁症与CMI特征的神经系统器质性疾病合并症所致，它可以改变免疫系统的状态。炎性介质在抑郁症形成和发展的病理生理机制中的作用的进一步分析将使更准确地确定客观风险标准和制定预防措施成为可能，这将有助于减少抑郁症对神经中毒总体状况的影响。这可能反映了对免疫应答的细胞因子调节机制的适当功能的干扰。细胞因子特征的显着变化可能是由于抑郁症与CMI特征的神经系统器质性疾病合并症所致，它可以改变免疫系统的状态。炎性介质在抑郁症形成和发展的病理生理机制中的作用的进一步分析将使更准确地确定客观风险标准和制定预防措施成为可能，这将有助于减少抑郁症对神经中毒总体状况的影响。细胞因子特征的显着变化可能是由于抑郁症与CMI特征的神经系统器质性疾病合并症所致，它可以改变免疫系统的状态。炎性介质在抑郁症形成和发展的病理生理机制中的作用的进一步分析将使更准确地确定客观风险标准和制定预防措施成为可能，这将有助于减少抑郁症对神经中毒总体状况的影响。细胞因子特征的显着变化可能是由于抑郁症与CMI特征的神经系统器质性疾病合并症所致，它可以改变免疫系统的状态。炎性介质在抑郁症形成和发展的病理生理机制中的作用的进一步分析将使更准确地确定客观风险标准和制定预防措施成为可能，这将有助于减少抑郁症对神经中毒总体状况的影响。