No abstract

The aim of the present study was to examine the effects of academic examination stress on leukocyte subset distribution in university students. Thirty-eight university students had repeated blood collections for white blood cell differentiation and flow cytometric assay of lymphocytic subsets a few weeks before and after (i.e. two baseline conditions) as well as the day before a difficult academic examination (i.e. stress condition). Flow cytometry was used to determine the number of peripheral blood mononuclear cells (PBMC). In students, who were reactors to psychological stress (criterion based on changes in the Perceived Stress Scale, PSS), but not in stress non-reactors, a significant increase in the number of neutrophils, monocytes, CD8⁺, CD2⁺CD26⁺, and CD2⁺HLA-DR⁺ T cells and CD19⁺ B cells, and significant reductions in the CD4⁺/CD8⁺ T cell ratio were observed in the stress condition. There were significant and positive relationships between the stress-induced changes in perceived stress (PSS scale) and number of leukocytes, neutrophils, CD2⁺, CD2⁺CD26⁺ and CD2⁺HLADR⁺ T cells, and CD19⁺ B cells. There were significant and negative relationships between the stress-induced changes in the CD4⁺/CD8⁺ ratio and the stress-induced changes in the PSS scale. Female students taking oral contraceptives showed significantly higher stress-induced responses in number of leukocytes, neutrophils and CD19⁺ B cells than male and female students without use of oral contraceptives. The results suggest that academic examination stress induces changes in the distribution of PBMC, which indicate immune activation and which are probably orchestrated by a stress-induced production of cytokines.

Effective treatment of severe or chronic unipolar depression requires the combination of pharmacological and psychotherapeutic interventions, and demands a theoretical paradigm integrating biological and psychosocial aspects of depression. Supported by recent research, we propose in our article a biopsychosocial diathesis-stress model of depression. Its basic aim is psychoeducational: to provide therapists, patients, and their environment a constructive conceptual framework to understand depressive complaints, vulnerability, and stress. The core of the model consists of the concept of psychobiological vulnerability, which is determined by risk factors-of a biogenetic, psychological, somatic, and societal nature-and by protective factors. Life events with an idiosyncratic, stress-inducing value interact with this vulnerability, triggering severe or chronic distress that affects the individual's resilience and leads to symptoms of depression. The pathogenesis of depression is symbolized by a negative downward loop, in which interactions among symptoms, vulnerability, and stressors drive the patient toward a depressive condition. Moreover, experiencing recurrent depression influences psychobiological vulnerability, the occurrence of stressors, and tremendously increases the risk of further relapse. The model stresses the self-evident integration of biological and psychological therapeutic interventions that need to focus on symptom reduction and on relapse prevention. Moreover, it offers the patient and therapist a psychoeducational context in which the individual's vulnerability and depressive symptoms can be treated. Finally, applications of the depression model as a therapeutic approach to severe depression in the phases of remoralization, symptom reduction, and relapse prevention are presented.