Neurophysiological and endocrine consequences of immune activity

Saphier, D.

doi:10.1016/0306-4530(89)90056-5

Cited by 47 publications

(9 citation statements)

References 77 publications

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“…Hypothalamic nuclei were initially screened and found to be reactive during the effector phase of the humoral immune response (days after inoculation) in anaesthetized [1] and in conscious rats [6,7,54,55]. We took advantage of two stereotypic bacterial antigens that elicit fast and well-characterized immune responses [25,56].…”

Section: Discussionmentioning

confidence: 99%

“…This discovery initiated the conceptualization of lymphocytes sharing a common chemical language with neurons for intra-and inter-system communication [2]. Surprisingly, however, after some attempts [3][4][5][6][7][8], only minor progress has been achieved in understanding the neural processing and encoding of lymphocyte signalling. Another provoking finding was the possibility to induce a behaviourally conditioned immune response employing antigens or immunomodulatory drugs as unconditioned stimuli [9].…”

Section: Introductionmentioning

confidence: 99%

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Electrical activity in rat cortico-limbic structures after single or repeated administration of lipopolysaccharide or staphylococcal enterotoxin B

et al. 2010

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Immune-to-brain communication is essential for an individual to aptly respond to challenging internal and external environments. However, the specificity by which the central nervous system detects or 'senses' peripheral immune challenges is still poorly understood. In contrast to post-mortem c-Fos mapping, we recorded neural activity in vivo in two specific cortico-limbic regions relevant for processing visceral inputs and associating it with other sensory signalling, the amygdala (Am) and the insular cortex (IC). Adult rats were implanted with deep-brain monopolar electrodes and electrical activity was monitored unilaterally before and after administration of two different immunogens, the T-cellindependent antigen lipopolysaccharide (LPS) or the T-cell-dependent antigen staphylococcal enterotoxin B (SEB). In addition, the neural activity of the same individuals was analysed after single as well as repeated antigen administration, the latter inducing attenuation of the immune response. Body temperature and circulating cytokine levels confirmed the biological activity of the antigens and the success of immunization and desensitization protocols. More importantly, the present data demonstrate that neural activity of the Am and IC is not only specific for the type of immune challenge (LPS versus SEB) but seems to be also sensitive to the different immune state (naive versus desensitization). This indicates that the forebrain expresses specific patterns of electrical activity related to the type of peripheral immune activation as well as to the intensity of the stimulation, substantiating associative learning paradigms employing antigens as unconditioned stimuli. Overall, our data support the view of an intensive immune-to-brain communication, which may have evolved to achieve the complex energetic balance necessary for mounting effective immunity and improved individual adaptability by cognitive functions.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Electrical activity in rat cortico-limbic structures after single or repeated administration of lipopolysaccharide or staphylococcal enterotoxin B

et al. 2010

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“…Cytokines produced by activated immune cells can alter neural activity [78,109], while hormones and neurotransmitters released by the nervous system can bind to receptors expressed by immune cells [15,110]. Based on the potent effects of IL-1ß on the brain and the association between pathological states of immune activation and depression, Smith [96], in 1991, proposed that excessive secretion of IL-1 and other macrophage products causes depression.…”

Section: Cytokines As a Mechanistic Framework For Cancer-related Sympmentioning

confidence: 99%

A Cytokine-Based Neuroimmunologic Mechanism of Cancer-Related Symptoms

Lee¹,

Dantzer

Langley

et al. 2004

Neuroimmunomodulation

266

184

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While many of the multiple symptoms that cancer patients have are due to the disease, it is increasingly recognized that pain, fatigue, sleep disturbance, cognitive dysfunction and affective symptoms are treatment related, and may lead to treatment delays or premature treatment termination. This symptom burden, a subjective counterpart of tumor burden, causes significant distress. Progress in understanding the mechanisms that underlie these symptoms may lead to new therapies for symptom control. Recently, some of these symptoms have been related to the actions of certain cytokines that produce a constellation of symptoms and behavioral signs when given exogenously to both humans and animals. The cytokine-induced sickness behavior that occurs in animals after the administration of infectious or inflammatory agents or certain proinflammatory cytokines has much in common with the symptoms experienced by cancer patients. Accordingly, we propose that cancer-related symptom clusters share common cytokine-based neuroimmunologic mechanisms. In this review, we provide evidence from clinical and animal studies that correlate the altered cytokine profile with cancer-related symptoms. We also propose that the expression of coexisting symptoms is linked to the deregulated activity of nuclear factor-kappa B, the transcription factor responsible for the production of cytokines and mediators of the inflammatory responses due to cancer and/or cancer treatment. These concepts open exciting new avenues for translational research in the pathophysiology and treatment of cancer-related symptoms.

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“…During an immune response, the electrophysiological activity of hypothalamic neurons increases [1][2][3]. There are concomitant changes in the metabolism of norepinephrine (NE) and serotonin (5-hydroxytryptamine, 5-HT) [4][5][6] as well as an activation of the hypothalamopituitary-adrenocortical (HPA) axis, elevating plasma concentrations of ACTH and corticosterone [7].…”

Section: Introductionmentioning

confidence: 99%

Catecholamine, Indoleamine and Corticosteroid Responses in Mice Bearing Tumors

Chuluyan

Wolcott²,

Chervenak³

et al. 2000

Neuroimmunomodulation

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The neurochemical and endocrine responses to inoculation of mice with the murine lymphoma cell line AW5E was studied. This cell line was chosen because it is NK cell lysis resistant and thus does not induce a normal immune response. Immune activation has long been known to be a potent stimulator of the hypothalamo-pituitary-adrenocortical (HPA) axis as well as brain catecholamine and indoleamine metabolism, involving increases in the brain concentrations of catabolites of norepinephrine (NE) and serotonin (5-HT), as well as free tryptophan. Mice injected intravenously with AW5E tumor cells exhibited small increases in plasma corticosterone and hypothalamic NE and 5-HT catabolites one day after injection. There were no significant changes after 6 or 8 days, but a sustained increase in hypothalamic NE and 5-HT metabolism appeared 10 days after injection. There were similar, but more limited changes in the brain stem and prefrontal cortex. On the last day tested (day 14), plasma corticosterone was slightly elevated, as were hypothalamic dopamine, NE and 5-HT catabolites and tryptophan. These results indicate that inoculation with AW5E tumor cells increases brain catecholamine and serotonin metabolism, the hypothalamus being the most sensitive region. The most marked increases occurred in the few days preceding death, and thus may be associated with the pathology of the tumor growth.

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Neurophysiological and endocrine consequences of immune activity

Cited by 47 publications

References 77 publications

Electrical activity in rat cortico-limbic structures after single or repeated administration of lipopolysaccharide or staphylococcal enterotoxin B

Electrical activity in rat cortico-limbic structures after single or repeated administration of lipopolysaccharide or staphylococcal enterotoxin B

A Cytokine-Based Neuroimmunologic Mechanism of Cancer-Related Symptoms

Catecholamine, Indoleamine and Corticosteroid Responses in Mice Bearing Tumors

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