Objectives: Insomnia is associated with physical and mental disorders. We examined the effect of insomnia on immune functions, focusing on the T helper 1 (Th1)/ T helper 2 (Th2) balance, by a cross-sectional design. Methods: We provided a self-administered questionnaire to evaluate sleep habits, smoking and medical disorders to 578 men without any toxic exposure (20–64 years old), and measured natural killer (NK) cell activity in 324 men and production of interferon-gamma (IFN-γ) and interleukin-4 (IL-4) after stimulation with phytohemagglutinin in 254 men. According to the criteria of DSM-IV, in which insomnia is classified into primary and secondary insomnia, we assessed the effect of insomnia on immune functions, controlling for age and smoking in groups with and without medical disorders. Results: The prevalence of insomnia in the present study was 9.2%. In the absence of medical disorders, insomniac men had a significantly lower IFN-γ and ratio of IFN-γ to IL-4 than noninsomniac men. Men with insufficient sleep or difficulty initiating sleep (DIS) had a significantly lower IFN-γ to IL-4 ratio than those not suffering from insufficient sleep or DIS. In the presence of medical disorders, insomniac men had significantly higher IL-4 than noninsomniac men. Men with difficulty maintaining sleep (DMS) had a significantly lower IFN-γ to IL-4 ratio than men without DMS. NK cell activity was independent of insomnia. Conclusions: The present results showed a link between insomnia unrelated to medical disorders and a shift in the Th1/Th2 balance toward Th2 dominance, indicating that the relationship between sleep quality and the etiology of immune-related diseases should be reconsidered.

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Objectives: Recent studies have shown that apoptosis is involved in stress responses. The present study examined if stressors increase in vitro apoptosis of peripheral blood T lymphocytes in a dose-dependent manner. Methods: Daily subjective stress was quantitatively analyzed in 40 nonsmoking men with a daily hassles questionnaire. Apoptosis of T lymphocytes was measured by flowcytometry using Annexin V/PI double staining method after 0, 12, and 24 h of culture in the presence or absence of dexamethasone (DEX). Using a cross-sectional design, the current study examined the relationship between stress and in vitro apoptosis of T cells. Results: Results showed that apoptosis of T lymphocytes in vitro has a significant correlation with stress and age. Stress was positively correlated with percentage of apoptosis in T cells after 12 h of culture, irrespective of DEX treatment. Age was positively correlated with the percentage of T cell apoptosis after 0 and 12 h of coculture with DEX. Conclusions: These results indicate that age-related apoptosis and stress-related apoptosis of T cells are modulated through different mechanisms. This is the first study to show that in vitro lymphocyte apoptosis is influenced by daily stress in a dose-dependent manner.

Background: Specific coping styles have been shown to modulate stress-induced immune alterations and influence actual health outcomes. This study examined the effects of stressors and coping styles on human T-cell subpopulations and in vitro cytokine production using a cross-sectional design. Methods: Seventy-one men (18–60 years old) were asked to complete a self-administered questionnaire that evaluates quantitative workload, mental demand and coping styles. The numbers of T-cell subpopulations and concentrations of interferon-γ (IFN-γ) and interleukin-4 (IL-4) after stimulation with phytohemaglutinin were measured. Results: Positive and negative coping were negatively related to IL-4 and the number of CD4+ cells, respectively. Interactions between positive coping and mental demand significantly affected the number of CD8+ cells, IFN-γ, IL-4 and the IFN-γ/IL-4 ratio. Among men reporting high mental demand, positive coping was related to increased IFN-γ and IFN-γ/IL-4. Among men reporting low mental demand, positive coping was related to a decreased number of CD8+ cells and lower concentrations of IFN-γ and IL-4. Analyses adjusting for the numbers of CD3+ and CD8+ cells revealed that the interactive effects of positive coping and mental demand on cytokine levels were attributable to the changes in T-cell function rather than the number of T cells. No modulating effect of anxiety on the associations of stressors and coping with immune function was observed. Depressive symptoms slightly, though not significantly, modulated the association of negative coping and the number of CD4+ cells. Conclusions: From the perspective of immunology, optimal stress characteristics were determined by an individual’s coping styles, with positive coping being associated with stress-induced changes in the number of CD8+ cells and in vitro cytokine production from T cells. Our findings suggest that it is important to consider the interactive effects of the complexity of work and the individual coping style in stress management.