Interleukin-1 in adrenal chromaffin cells

Schultzberg, Marianne; Andersson, Charlotte; Undén, Anders; Troye‐Blomberg, Marita; Svenson, Stefan B.; Bartfai, Tamás

doi:10.1016/0306-4522(89)90171-1

Cited by 89 publications

(38 citation statements)

References 17 publications

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“…Taken together, the elevation of corticosterone after acute morphine treatment does not appear to be the adrenal cortical factor that increases plasma IL-6. A second potential adrenal-derived factor is the proinflammatory cytokine IL-1␤, which is localized within the adrenal cortex (Schultzberg et al, 1989) and stimulates the release of IL-6 from adrenal cortical cells (Judd and MacLeod, 1995) as well as many other tissues (for review, see Heinrich et al, 1990). Acute morphine treatment to mice has been shown to increase IL-1␤ and tumor necrosis factor-␣ levels released from phytohemagglutinin-stimulated splenocyte cultures (Pacifici et al, 2000), yet it is unknown whether this elevation also occurs in the adrenal gland.…”

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Rapid Elevation of Plasma Interleukin-6 by Morphine Is Dependent on Autonomic Stimulation of Adrenal Gland

Houghtling

Bayer²

2002

The Journal of Pharmacology and Experimental Therapeutics

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Several studies have demonstrated that opioids regulate a number of immune cell functions either through direct mechanisms or through the modulation of central nervous system outputs. It has been previously shown that morphine increases serum interleukin-6 (IL-6) levels; however, the mechanism by which this effect is produced is unknown. In the present study, experiments were designed to address the potential role of central opioid receptors, peripheral autonomic ganglia, and activation of the adrenals in the elevation of plasma IL-6 after morphine administration. A rapid and significant (2-fold) increase in plasma IL-6 was observed after morphine administration (10 mg/kg s.c.) to rats. This effect of morphine peaked within 30 min and remained elevated for at least 2 h. Central microinjection of morphine (10 g/2 l i.c.v.) mimicked the effects of peripherally administered morphine and was completely blocked by naltrexone (10 mg/kg s.c.) pretreatment. Pretreatment with a ganglionic blocker, chlorisondamine (0.5 mg/kg i.p.), also blocked the elevation of IL-6 by morphine, suggesting a role of the autonomic nervous system. In adrenalectomized animals, morphine administration did not increase IL-6 levels, whereas in adrenal demedullated animals, the effect of morphine remained intact. Thus, the adrenal cortex may be a potential source of IL-6, because IL-6 mRNA has been localized in the adrenal gland. Collectively, these data suggest a unique mechanism by which stimulation of central opioid receptors results in the elevation of plasma IL-6 through autonomic activation specifically of the adrenal cortex.

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confidence: 99%

Rapid Elevation of Plasma Interleukin-6 by Morphine Is Dependent on Autonomic Stimulation of Adrenal Gland

Houghtling

Bayer²

2002

The Journal of Pharmacology and Experimental Therapeutics

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“…Adrenal chromaffin cells synthesize and store large amounts separate chromaffin cells (Hillarp &MHkfelt, 1953; Bartfai, 1989). The proportions proportion of the total.…”

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Differential secretion of catecholamines in response to peptidergic and cholinergic transmitters in rat adrenals.

Guo

Wakade

1994

The Journal of Physiology

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1. Rat adrenal medulla is stimulated by cholinergic and peptidergic transmitters released from splanchnic nerves. The peptidergic transmitter has been identified as vasoactive intestinal polypeptide (VIP) and its contribution in comparison to that of acetylcholine (ACh) is more prominent at low neuronal activity. The purpose of this study is to determine if ACh and VIP cause differential secretion of adrenaline and noradrenaline and whether the differential secretion also occurs when splanchnic nerves are stimulated at different frequencies. 4. Perfusion with VIP (10 FM for 4 min) resulted in the secretion of 27 ng of catecholamines and the ratio of adrenaline to noradrenaline was 9-7. A higher concentration of VIP (20 FM for 4 min) resulted in the secretion of greater amounts of catecholamines (102 ng) without significantly altering the ratio of adrenaline to noradrenaline (10-9). 5. Perfusion with as low as 0 01 uM pituitary adenylate cyclase-activating polypeptide (PACAP) increased the secretion of catecholamines to 31 ng and the secretion increased in a dose-dependent manner up to 0 3 FM. The ratio of adrenaline to noradrenaline was 6-8 with 0 1 FM PACAP and remained almost unchanged throughout the concentration range. 6. Electrical field stimulation at 0-5 Hz for 300 s resulted in the secretion of 34 ng catecholamines, and the ratio of adrenaline to noradrenaline was 6-9. Delivering the same number of pulses at 1 Hz increased the secretion to 42 ng but reduced the ratio to 6 3. Increasing stimulation frequency to 10 Hz for 15 s or 30 s further increased the secretion to 66 ng and 180 ng, respectively, but significantly reduced the ratio to about 5. 7. Delivery of same number pulses at 3 Hz continuously or at 30 Hz in bursts caused a substantial reduction in catecholamine secretion (55 versus 35 ng) and in the ratio of adrenaline to noradrenaline (7 4 versus 5). 8. These results agree with the hypothesis that cholinergic and peptidergic transmitters control catecholamine secretion at different levels of neuronal activity and provide new evidence that ACh stimulates the secretion of noradrenaline and adrenaline whereas VIP and PACAP predominantly stimulate the secretion of adrenaline.

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“…Similarly, ACTH (a proximal mediator of HPA activity) has been shown to stimulate the release of IL-1 and IL-6 from cells in the zona glomerulosa of the adrenal cortex [16][17][18]. Furthermore, the adrenal medulla has been shown to produce both IL-1 and IL-6 [19][20][21]. Thus, direct release of cytokines during stress may represent one pathway by which stressors alter immune function.…”

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confidence: 99%

Acute Stress May Facilitate Recovery from a Subcutaneous Bacterial Challenge

Deak¹,

Nguyen²,

Fleshner

et al. 1999

Neuroimmunomodulation

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The effects of stress on the immune system vary with both the duration and type of stressor. Many studies suggest that stress may compromise an organism’s ability to recover from immune challenge. However, recent findings suggest that stress may actually enhance some aspects of immune function. For example, exposure to a single session (∼2 h) of intermittent inescapable tailshocks (IS) has been shown to activate the acute phase response and increase some aspects of macrophage function. Thus, the following experiments assessed whether IS exposure would alter local inflammation produced by peripheral injection of streptomycin-killed bacteria. Rats (Harlan Sprague Dawley) were exposed to IS (100 1.6-mA, 60 s variable intertrial interval) and injected with Escherichia coli (∼2.5 × 10⁸ CFU s.c. posterior to the shoulder blades). The area of inflammation was measured until the inflammation had completely resolved (typically 7–8 days). When bacteria were administered immediately after IS, rats resolved inflammation significantly faster than did nonstressed rats. Since adrenalectomy did not reduce the effect of IS, it is unlikely that this effect is a result of elevated corticosterone levels. Furthermore, IS does not appear to alter the rat’s ability to sequester bacteria in the subcutaneous space since no swelling of lymph nodes or chronic activation of the hypothalamic-pituitary-adrenal axis was observed.

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Interleukin-1 in adrenal chromaffin cells

Cited by 89 publications

References 17 publications

Rapid Elevation of Plasma Interleukin-6 by Morphine Is Dependent on Autonomic Stimulation of Adrenal Gland

Rapid Elevation of Plasma Interleukin-6 by Morphine Is Dependent on Autonomic Stimulation of Adrenal Gland

Differential secretion of catecholamines in response to peptidergic and cholinergic transmitters in rat adrenals.

Acute Stress May Facilitate Recovery from a Subcutaneous Bacterial Challenge

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