Neuroimmunomodulation: facts and dilemmas

Janković, Branislav D.

doi:10.1016/0165-2478(89)90046-1

Cited by 67 publications

(35 citation statements)

References 115 publications

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“…Electrolytic lesions of certain areas of the hypothalamus produce either enhancement or inhibition of various immune functions (25). These changes, both facilitatory and inhibitory, are prevented by hypophysectomy, indicating that pituitary function mediates the hypothalamic effect (28).…”

mentioning

confidence: 95%

“…The facts that both the hypothalamus and the pituitary gland can produce both immune-enhancing and immunesuppressive effects and, furthermore, that the pituitary is under hypothalamic control provide a mechanism for tightly regulating the immune response in both magnitude and duration (2). Further evidence for a CNS-immune system interaction is derived from the observation that certain neurotransmitters, neuropeptides, and neurohormones affect immune function both in vivo and in vitro; receptors for these molecules are present on lymphocytes and/or macrophages (7,25). Cytokines, in turn, elaborated from activated immune cells can alter HPA axis function, thereby closing a negative-feedback loop.…”

mentioning

confidence: 99%

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Central nervous system-immune system interactions: psychoneuroendocrinology of stress and its immune consequences

Black

1994

Antimicrob Agents Chemother

165

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Psychoneuroimmunology is a relatively new discipline which deals with CNS-immune system interactions. The evidence for such interactions was reviewed, as was the neuroendocrinologic response to stress. Recent evidence indicates that the behavioral, nervous system, and neuroendocrine responses to stress are mediated by hypothalamic CRF, which acts on both the sympathetic nervous system and the HPA axis, resulting in increased levels of corticosteroids, catecholamines, and certain opiates, substances which are generally immunosuppressive. Concentrations of growth hormone and prolactin, which are immunoenhancing, are elevated early during the response to stress but are later suppressed. Although several other neuromediators may also be released with stress, the net effect of a variety of acute stressors is down regulation of the immune system function. In the following minireview, I consider whether stress alters the resistance of the host to infection as well as the immunomodulatory effects of released immune system mediators on the brain.

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mentioning

confidence: 95%

mentioning

confidence: 99%

Central nervous system-immune system interactions: psychoneuroendocrinology of stress and its immune consequences

Black

1994

Antimicrob Agents Chemother

165

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“…I now consider whether and how products of immune cells are released and influence the brain. It has long been known that inoculation of foreign antigens induces a classic stress response in animals (18,32), with elevated corticosteroid (22,47) and catecholamine levels and increased catecholamine turnover in the brain and periphery (4,22). The levels of circulating corticosteroids were maximal at the peak of an immune response to an antigenic challenge (5,47).…”

Section: Immune System-brain Interactionsmentioning

confidence: 99%

Immune system-central nervous system interactions: effect and immunomodulatory consequences of immune system mediators on the brain

Black

1994

Antimicrob Agents Chemother

111

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The field of psychoneuroimmunology deals with brainimmune system interactions. Studies involving various stress paradigms have revealed that the brain can influence the immune system through its various neuropeptides, neurohormones, and neurotransmitters. In the accompanying minireview (6), the consequences of stress on the immune system were reviewed; in general, immune suppression results from acute stress (6).Substantial animals responding with a large antibody immune response, as determined by a greater plaque-forming capacity of B cells, had more norepinephrine depletion in the hypothalamic and brain stem nuclei (34). These findings of stimulated norepinephrine metabolism and turnover were thought to be indicative of increased neurogenic activity of neurons containing norepinephrine (34). They were similar to those seen with stress and were likely to be due to stimulation of neurons that release corticotropin-releasing factor (CRF), with the subsequent activation by CRF of sympathetic nuclei in the hypothalamus and locus ceruleus. I now consider the likely mechanism(s) that is responsible for these changes in corticosteroid and norepinephrine metabolism. CYTOKINES AND THE CRF RESPONSEIt is now known that cytokines such as interleukin-1 (IL-1), tumor necrosis factor alpha (TNF-a), and IL-6, which are released from immune cells, specifically, macrophages during immune system activation, affect the brain. Although a blood-brain barrier exists to exclude watersoluble substances such as circulating peptides and proteins from the brain, this barrier is lacking in the area of the preoptic nucleus of the hypothalamus (1, 57). Certain neurons in the preoptic nucleus have receptors for IL-1, TNF-a, and IL-6, to which the cytokines bind and thereby pass from the circulation to the brain (57). Preoptic neurons communicate with another hypothalamic nucleus, the paraventricular nucleus, which contains neurons that release CRF. As described in the accompanying minireview (6)

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“…We designed the experiments described below in order to accomplish the following: (1) to determine the critical hypothalamic area associated with the immune depression that followed lesioning; (2) to ascertain the effects of those lesions on the size and structure of lymphoid organs and on lymphocyte toxicity; and (3) to verify whether changes in the structure and function of lymphoid organs were secondary to food deprivation or to changes in corticosterone levels.…”

Section: Introductionmentioning

confidence: 99%

“…Peripheral immune mechanisms have been investigated to a great extent but the neural structures that play a role in such regulation have not been fully identified. 1 Brain immune interactions have an important role in the pathophysiology of diseases such as multiple sclerosis, neuroAIDS, and Alzheimer's, which are highly prevalent and have a profound social cost. [2][3][4][5][6][7][8][9] Several studies have demonstrated that the central nervous system participates in the regulation of immune function.…”

Section: Introductionmentioning

confidence: 99%

Circumscribed lesion of the medial forebrain bundle area causes structural impairment of lymphoid organs and severe depression of immune function in rats

Timo-Iaria

et al. 1998

Mol Psychiatry

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Interactions between the immune system and the brain are a key element in the pathophysiology of diseases such as multiple sclerosis, neuroAIDS, and Alzheimer's, which affect large numbers of individuals and are associated with a high social cost. However, the neuroanatomical basis of brain-immune interactions has not been elucidated. We report that in Wistar rats of either sex bilateral electrolytic lesion of the medial forebrain bundle reduces body weight by 28% 7 days after lesioning, and causes widespread infections, aphagia, adypsia, structural damage to the lymphoid organs and heavy depression of T lymphocytes cytotoxicity. The following alterations occur in the immune system after those lesions: the weight of the thymus, spleen and lymphonodes is reduced by 77.9%, 49.1% and 48.4%, respectively. The thymus is atrophied and contains fewer lymphoid cells in the cortex than in the medulla. In the spleen the white pulp is reduced and lymphoid cells from periarteriolar zones and at the chords are almost absent. In lymph nodes cortical small lymphocytes are depleted and primary and secondary nodules and germinal centers all but disappear. Cytotoxicity of lymphocytes is reduced by 86.2% in the thymus, 77.6% in the spleen and 70.2% in lymph nodes. The critical area of lesion is at the medialmost portion of the medial forebrain bundle, at the preoptic area and rostral part of the anterior hypothalamus. We suggest that this area contains neural circuits that are crucial for keeping the structure of lymphoid organs and the functional integrity of the immune system.

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Neuroimmunomodulation: facts and dilemmas

Cited by 67 publications

References 115 publications

Central nervous system-immune system interactions: psychoneuroendocrinology of stress and its immune consequences

Central nervous system-immune system interactions: psychoneuroendocrinology of stress and its immune consequences

Immune system-central nervous system interactions: effect and immunomodulatory consequences of immune system mediators on the brain

Circumscribed lesion of the medial forebrain bundle area causes structural impairment of lymphoid organs and severe depression of immune function in rats

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