Interaction Between The Brain And Immune System In Stress And Depression

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The monoamine hypothesis of depression proposes that a deficit of brain noradrenaline (NA) and/or serotonin (5-HT) may be causally involved in the symptoms of illness (Baldessarini (1975). Another theory of depression suggests that the disorder in hypothalamus-pituitary-adrenal (HPA) axis causes an increase in secretion of corti-cotropin-releasing factor (CRF), which stimulates adrenocorticotrophin hormone (ACTH) and Cortisol release (Bateman Singh, Krai, and Solomon, 1989). Recently, the macrophage theory of depression, which will be discussed in detail later in this review, has also been proposed. In this hypothesis, the abnormal secretion of some cytokines such as interleukin-1 (IL-1) and interferon-alpha (INF-alpha), results in disordered secretions of CRF, ACTH, prolactin, and Cortisol, together with a depressive state (Smith, (1991). These three hypothesis may be linked. Whatever changes in the central nervous system (CNS) or in the endocrine system occur, different aspects of immune function are affected. It is known that noradrenergic and cholinergic terminals innervate the thymus gland and bone marrow and there are different neuropeptide, neurotransmitter and hormone receptors on lymphocytes and monocytes. In addition, cytokines produced by immune cells and microglia exert different effects on the brain and on the endocrine and immune systems (Bost, 1988; Farrar, 1988).

A number of studies have shown that stress and depression are often associated with an impairment in immune function (Kronfol and House, 1989). At the cellular level, a reduction in mitogen-stimulated lymphocyte proliferation and neutrophil phagocytosis and elevated monocyte activity has been reported in stress and depression (Leonard, 1990; McAdams and Leonard, 1993; O'Neill and Leonard, 1990). An increase in total white cell number and an abnormality in differential white blood cell (WBC) count (for example, increase in the percentage of neutrophil and decrease in lymphocytes) has also been found after stress or in depressed patients (Maes, Planken, and Stevens, 1992). Recently, leucocyte adhesiveness/aggregation (LAA) has also been reported to be increased during stress; this has been suggested as a marker of stress (Arber, Berliner, and Tamir, 1991).

At the subcellular level, it has been reported that serum and plasma concentrations of immunoglobulin (Ig) complement (C) and acute phase proteins are changed in depressed patients (Healy, 1991; Kronfol and House, 1989; Maes et al. 1992). For example, IgA, IgM, complement C3, C4, and positive acute phase proteins are increased in depression, while negative acute phase proteins are decreased (Song, Dinan, and Leonard, 1994). The concentrations of cytokines IL-1, INF-alpha, and tumor necrosis factor are raised and IL-2 is reduced in the depressed patient (Katila, Rimon, Cantwell, Appelberg, and Nikkila, 1991; Nathan, 1987; Smith, 1991). At the organ and system level, it has been reported that the weights of thymus gland and spleen are reduced and adrenal is increased during stress (Dohmus and Metz, 1991). Histological studies reveal that a stress-induced rise in corticosterone, or an exogenous injection of corti-costerone, causes cortical atrophy and lymphocyte necrosis in the thymus gland of rats (Dohmus and Metz (1991). However, despite the circumstantial evidence implicating an interaction between neurotransmitter, endocrine, and immune changes, a causal relationship between these changes has yet to be proven.

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