Subdiaphragmatic vagotomy inhibits intra-abdominal interleukin-1β stimulation of adrenocorticotropin secretion

Kapcala, Leonard P.

doi:10.1016/s0006-8993(96)00511-2

Cited by 17 publications

(27 citation statements)

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“…Peripheral cytokines affect the central nervous system either by activating peripheral vagal afferents which project to the amygdala and the hippocampus through the nucleus tractus solitaries [103][104][105][106]. This mechanism then activates the release of brain derived cytokines from glia or astrocytes.…”

Section: Cytokinesmentioning

confidence: 99%

Heart failure and cognitive dysfunction

Ampadu

Morley

2015

International Journal of Cardiology

147

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Section: Cytokinesmentioning

confidence: 99%

Heart failure and cognitive dysfunction

Ampadu

Morley

2015

International Journal of Cardiology

147

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“…IL‐1 β ( 8), ACTH release after 20 μg/kg i.p. IL‐1 β ( 9), and to abolish ACTH secretion after 4 μg/kg i.p. IL‐1 β ( 9).…”

Section: Discussionmentioning

confidence: 99%

“…IL‐1 β , there is increasing evidence that the integrity of vagal sensory afferent fibres is critical for many of the responses observed following i.p. injection of IL‐1 β , including HPA axis activation ( 8, 9). There appears to be some specificity in the type of vagal afferents involved, since a complete subdiaphragmatic vagotomy, which includes disruption of gastric vagal afferents, appears to be effective in inhibiting the effects of i.p.…”

mentioning

confidence: 99%

Evidence that Cholecystokinin Receptors are not Involved in the Hypothalamic‐Pituitary‐Adrenal Response to Intraperitoneal Administration of Interleukin‐1β

Day

Akil

1999

J Neuroendocrinology

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The purpose of this study was to investigate a putative role for cholecystokinin (CCK) in the activation of the hypothalamic-pituitary-adrenal (HPA) axis following intraperitoneal (i.p.) administration of interleukin-1-beta (IL-1beta). Previous studies predict that CCKA receptors on vagal sensory afferents may be involved in the initiation of the stress response following an acute i.p. injection of IL-1beta. Adult male rats were given an i.p. injection of a specific CCKA (devazepide, 1 mg/kg) or CCKB (CI-988, 1 mg/kg) receptor antagonist, 30 min prior to an i.p. injection of rat recombinant IL-1beta (rrIL-1beta), 0.5 microg/kg in 0.9% sterile saline/0.01% rat serum albumin. Blood samples were obtained via an indwelling jugular vein catheter, and the plasma levels of the stress hormones ACTH (adrenocorticotropin hormone) and corticosterone analysed over time as an indicator of HPA axis activation. This dose of rrIL-1beta resulted in a significant release of ACTH and corticosterone, peaking at 30-60 min, and returning to basal levels by 2 h. Pretreatment with either devazepide or CI-988 had no effect on the rrIL-1beta induced ACTH or corticosterone release. In contrast, the same dose of devazepide completely inhibited the ACTH and corticosterone response to i.p. CCK (octapeptide, sulphated form, CCK-8S), 5 microg/kg. It is concluded that CCK receptors are not involved in the hormonal stress response to a submaximal i.p. dose of rrIL-1beta.

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“…These nuclei integrate sensory signals and control visceral reflexes, and also relay visceral sensory information to the central autonomic network [127]. Subdiaphragmatic vagotomy inhibits activation of the paraventricular nucleus and subsequent secretion of ACTH in response to lipopolysccharides and IL-1 [128,129]. …”

Section: Regulation Of the Cns By The Immune Systemmentioning

confidence: 99%

Untitled

2003

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251 ACTH = adrenocorticotropin; AVP = arginine vasopressin; CNS = central nervous system; CRH = corticotropin-releasing hormone; DHEA = dehydroepiandrosterone; GH = growth hormone; GR = glucocorticoid receptor; HPA = hypothalamic-pituitary-adrenal; HPG = hypothalamicpituitary-gonadal; HPT = hypothalamic-pituitary-thyroid; IFA = incomplete Freund's adjuvant; IGF = insulin-like growth factor; IL = interleukin; NF-κB = nuclear factor-κB; PBMCs = peripheral blood mononuclear cells; RA = rheumatoid arthritis; T 3 = triiodothyronine; T 4 = thyroxine; Th = T helper cells; TNF = tumor necrosis factor; TRH = thyrotropin-releasing hormone; TSH = thyroid-stimulating hormone.Available online http://arthritis-research.com/content/5/6/251 IntroductionThe inflammatory response is modulated in part by a bidirectional communication between the brain and the immune systems. This involves hormonal and neuronal mechanisms by which the brain regulates the function of the immune system and, in the reverse, cytokines, which allow the immune system to regulate the brain. In a healthy individual this bidirectional regulatory system forms a negative feedback loop, which keeps the immune system and central nervous system (CNS) in balance. Perturbations of these regulatory systems could potentially lead to either overactivation of immune responses and inflammatory disease, or oversuppression of the immune system and increased susceptibility to infectious disease. Many lines of research have recently established the numerous routes by which the immune system and the CNS communicate. This review will focus on these regulatory systems and their involvement in the pathogenesis of inflammatory diseases such as rheumatoid arthritis (RA). For other reviews on the involvement of these regulatory pathways in RA and other inflammatory diseases, see reviews by Eijsbouts and Murphy There are two major pathways by which the CNS regulates the immune system: the first is the hormonal response, mainly through the hypothalamic-pituitaryadrenal (HPA) axis, as well as the hypothalamic-pituitary-gonadal (HPG), the hypothalamic-pituitary-thyroid (HPT) and the hypothalamic-growth-hormone axes; the second is the autonomic nervous system, through the release of norepinephrine (noradrenaline) and acetylcholine from sympathetic and parasympathetic nerves. In turn, the immune system can also regulate the CNS through cytokines. Review Neural immune pathways and their connection to inflammatory diseases AbstractInflammation and inflammatory responses are modulated by a bidirectional communication between the neuroendocrine and immune system. Many lines of research have established the numerous routes by which the immune system and the central nervous system (CNS) communicate. The CNS signals the immune system through hormonal pathways, including the hypothalamic-pituitary-adrenal axis and the hormones of the neuroendocrine stress response, and through neuronal pathways, including the autonomic nervous system. The hypothalamic-pituitary-gonadal axis and sex hormones a...

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Subdiaphragmatic vagotomy inhibits intra-abdominal interleukin-1β stimulation of adrenocorticotropin secretion

Cited by 17 publications

References 0 publications

Heart failure and cognitive dysfunction

Heart failure and cognitive dysfunction

Evidence that Cholecystokinin Receptors are not Involved in the Hypothalamic‐Pituitary‐Adrenal Response to Intraperitoneal Administration of Interleukin‐1β

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