Interleukin-I immunoreactive innervation of the human hypothalamus

Department of Pediatrics, Tufts University, Бостон, Georgia, United States
Science (Impact Factor: 33.61). 05/1988; 240(4850):321-4. DOI: 10.1126/science.3258444
Source: PubMed


Interleukin-1 (IL-1) is a cytokine that mediates the acute phase reaction. Many of the actions of IL-1 involve direct effects on the central nervous system. However, IL-1 has not previously been identified as an intrinsic component within the brain, except in glial cells. An antiserum directed against human IL-1 beta was used to stain the human brain immunohistochemically for IL-1 beta-like immunoreactive neural elements. IL-1 beta-immunoreactive fibers were found innervating the key endocrine and autonomic cell groups that control the central components of the acute phase reaction. These results indicate that IL-1 may be an intrinsic neuromodulator in central nervous system pathways that mediate various metabolic functions of the acute phase reaction, including the body temperature changes that produce the febrile response.

3 Reads
  • Source
    • "Notably, these regions might be involved in the regulation of sleep. Further, IL-1í µí»½ has effects on the serotonergic system and governs sleep at several levels [35] [36] [37]. This evidence implicates an interaction between components of the immune system and the mechanisms that generate sleep. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Sleep is considered an important modulator of the immune response. Thus, a lack of sleep can weaken immunity, increasing organism susceptibility to infection. For instance, shorter sleep durations are associated with a rise in suffering from the common cold. The function of sleep in altering immune responses must be determined to understand how sleep deprivation increases the susceptibility to viral, bacterial, and parasitic infections. There are several explanations for greater susceptibility to infections after reduced sleep, such as impaired mitogenic proliferation of lymphocytes, decreased HLA-DR expression, the upregulation of CD14+, and variations in CD4+ and CD8+ T lymphocytes, which have been observed during partial sleep deprivation. Also, steroid hormones, in addition to regulating sexual behavior, influence sleep. Thus, we hypothesize that sleep and the immune-endocrine system have a bidirectional relationship in governing various physiological processes, including immunity to infections. This review discusses the evidence on the bidirectional effects of the immune response against viral, bacterial, and parasitic infections on sleep patterns and how the lack of sleep affects the immune response against such agents. Because sleep is essential in the maintenance of homeostasis, these situations must be adapted to elicit changes in sleep patterns and other physiological parameters during the immune response to infections to which the organism is continuously exposed.
    Journal of Immunology Research 01/2015; 2015(4):1-14. DOI:10.1155/2015/678164 · 2.93 Impact Factor
  • Source
    • "Indeed, IL-1 has been shown to influence hypothalamic neurosecretory activity by stimulating CRH release by hypothalamic CRH neurons, and to enhance the turnover of NE in the hypothalamus (84, 85). IL-1 is also produced by several type of cells resident in the CNS, including astrocytes and microglia (86, 87) and IL-1 receptors have been identified in different brain areas, such as hippocampus and the dorsal raphe nucleus (88, 89). Furthermore, mRNA for IL-1α and TNF-α has been demonstrated in anterior pituitary cells (90, 91), which secrete IL-6 as well (91). "
    [Show abstract] [Hide abstract]
    ABSTRACT: The nervous and immune systems have long been considered as compartments that perform separate and different functions. However, recent clinical, epidemiological, and experimental data have suggested that the pathogenesis of several immune-mediated disorders, such as multiple sclerosis (MS), might involve factors, hormones, and neural mediators that link the immune and nervous system. These molecules are members of the same superfamily, which allow the mutual and bi-directional neural-immune interaction. More recently, the discovery of leptin, one of the most abundant adipocyte-derived hormones that control food intake and metabolism, has suggested that nutritional/metabolic status, acting at central level, can control immune self-tolerance, since it promotes experimental autoimmune encephalomyelitis, an animal model of MS. Here, we summarize the most recent advances and the key players linking the central nervous system, immune tolerance, and the metabolic status. Understanding this coordinated interaction may pave the way for novel therapeutic approaches to increase host defense and suppress immune-mediated disorders.
    Frontiers in Immunology 04/2014; 5:143. DOI:10.3389/fimmu.2014.00143
  • Source
    • "NF-κB activation is important for TNF-α secretion from Schwann cells and may play a key role in triggering positive-feedback loops for IL-6 expression [39]. Neurons can synthesize and express molecular inflammatory mediators, and these cytokines may participate in neuronal communication [40], [41], [42]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Tumor necrosis factor-α plays important roles in immune system development, immune response regulation, and T-cell-mediated tissue injury. The present study assessed the net value of anti-tumor necrosis factor-α treatment in terms of functional recovery and inhibition of hypersensitivity after peripheral nerve crush injury. We created a right sciatic nerve crush injury model using a Sugita aneurysm clip. Animals were separated into 3 groups: the first group received only a skin incision; the second group received nerve crush injury and intraperitoneal vehicle injection; and the third group received nerve crush injury and intraperitoneal etanercept (6 mg/kg). Etanercept treatment improved recovery of motor nerve conduction velocity, muscle weight loss, and sciatic functional index. Plantar thermal and von Frey mechanical withdrawal thresholds recovered faster in the etanercept group than in the control group. On day 7 after crush injury, the numbers of ED-1-positive cells in crushed nerves of the control and etanercept groups were increased compared to that in the sham-treated group. After 21 days, ED-1-positive cells had nearly disappeared from the etanercept group. Etanercept reduced expression of interleukin-6 and monocyte chemotactic and activating factor-1 at the crushed sciatic nerve. These findings demonstrate the utility of etanercept, in terms of both enhancing functional recovery and suppressing hypersensitivity after nerve crush. Etanercept does not impede the onset or progression of Wallerian degeneration, but optimizes the involvement of macrophages and the secretion of inflammatory mediators.
    PLoS ONE 02/2013; 8(2):e57721. DOI:10.1371/journal.pone.0057721 · 3.23 Impact Factor
Show more