Neutrophilia and lymphopenia in major mood disorders

Darko, Denis F.; Rose, James D.; Gillin, J. Christian; Golshan, Shahrokh; Baird, Stephen M.

doi:10.1016/0165-1781(88)90095-9

Cited by 65 publications

(30 citation statements)

References 19 publications

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“…who found that depressed patients (espe cially the highly stressed) exhibited increased total leuko cyte and lymphocyte numbers. Like Darko et al [30], we observed that the number of CD4+ lymphocytes was higher in the peripheral blood of depressed patients as opposed to control subjects. However, no difference in the CD4+/CD8+ ratio could be detected in our study, whereas Darko et al [32] found a higher ratio in the depressed patients.…”

Section: Discussionsupporting

confidence: 60%

Immune Disturbances during Major Depression: Upregulated Expression of Interleukin-2 Receptors

Bosmans²,

et al. 1990

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We determined the following immune parameters in drug-free, major depressed patients and in age- and sex-matched healthy controls: the number and percentage of interleukin-2 receptor (IL-2R) bearing cells (CD25⁺, anti-TAC), serum circulating levels of soluble (s)IL-2Rs, the pre- and postdexamethasone phytohemagglutinin (PHA)-induced accumulation of sIL-2Rs in culture supernatant, and the number of T helper (CD4⁺) and T suppressor (CD8⁺) cells. In comparison with normal volunteers, patients with major depression had a higher number and percentage of CD25⁺ cells, higher concentrations of serum circulating sIL-2Rs, higher supernatant sIL-2Rs after stimulation with PHA, and a higher number of CD4⁺ cells. The CD4⁺/CD8⁺ ratio and the number of CD4⁺ cells were significantly and positively related to the number of cells expressing the CD25⁺ antigen. These results may indicate that depressed patients display an increased number of T cells in an early phase of activation.

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Section: Discussionsupporting

confidence: 60%

Immune Disturbances during Major Depression: Upregulated Expression of Interleukin-2 Receptors

Bosmans²,

et al. 1990

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“…Typically, investigators have focused on clinical disorders, e.g., major depressive disorders; the results of these studies have been contradictory (1)(2)(3)(4)(5)(6)(7)(8). Studies on individuals with "pathological affect" may not be relevant to the question of immune alterations during normal mood.…”

Section: Introductionmentioning

confidence: 99%

Immunological and physiological changes associated with induced positive and negative mood.

Futterman

Kemeny

Shapiro

et al. 1994

Psychosomatic Medicine

104

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Functional and phenotypic immunological parameters were examined before, at the end of, and 20 minutes after the induction of positive and negative mood states, varied for arousal level, and a neutral state. The subjects were 14 male actors who experienced each condition on a different day. Compared with a neutral condition, all mood states affected several immune parameters (e.g., natural killer cell percentage and activity and percentage of suppressor/cytotoxic T cells), regardless of the valence or arousal level of the mood induced. The only immune variable differentially sensitive to positive and negative mood states was the proliferative response to the mitogen phytohemagglutinin; the response increased after positive moods and decreased after negative moods. Analysis of covariance for repeated measures indicated that heart rate, alone or in combination with physical activity and cortisol levels, had an impact on mood effects for most of the immune parameters investigated.

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“…As reported (Szuster-Ciesielska et al, 2008), patients with major depression exhibit accelerated apoptosis of leukocytes and blood oxidative stress levels resulting in fewer T-helper lymphocytes and neutrophils and an rise in reactive oxygen species (ROS) generation, infections, and pro-apoptotic proteins. This may explain the reduction in the number of lymphocytes in peripheral blood of these patients (Darko et al, 1988;Kronfol et al, 1985). We propose that the immunodeficiency of depressive patients (Leonard and Myint, 2009) is not an intrinsic immunodeficiency but rather a consequence of the extensive T-cell activation-adhesion and oxidative stress.…”

Section: Depressionmentioning

confidence: 93%

Melatonin as a potential therapeutic agent in psychiatric illness

Maldonado

Reíter

Pérez-San-Gregorio

2009

Human Psychopharmacology

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The aim of this review was to summarize the potential use of melatonin in the treatment of mental disorders, specifically bipolar disorders, depression, and schizophrenia. To date, melatonin has been most commonly used in psychiatry because of its hypnotic, rhythm resynchronizing, and antioxidant actions. Here, we examine other properties of the melatonin including its anti-inflammatory, antinociceptive, anxiolytic, and drug detoxification actions as well as its protective effects against neural loss. The brain is an intricate sensory and motor organ which receives information from both the external and internal environments. It transduces information into complex chemical and electrical signals which are transmitted throughout the central nervous system (CNS) and the organism. The pathogenesis of mental disorders remains ambiguous and neuroinflammation has been proposed as a causative agent. We consider the potential contributions of melatonin as therapeutic agent in CNS and during neuroinflammation in mental disorders.

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Neutrophilia and lymphopenia in major mood disorders

Cited by 65 publications

References 19 publications

Immune Disturbances during Major Depression: Upregulated Expression of Interleukin-2 Receptors

Immune Disturbances during Major Depression: Upregulated Expression of Interleukin-2 Receptors

Immunological and physiological changes associated with induced positive and negative mood.

Melatonin as a potential therapeutic agent in psychiatric illness

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