Evidence that shock-induced immune suppression is mediated by adrenal hormones and peripheral β-adrenergic receptors

Cunnick, Joan E.; Lysle, Donald T.; Kucinski, Barbara J.; Rabin, Bruce S.

doi:10.1016/0091-3057(90)90270-r

Cited by 151 publications

(53 citation statements)

References 25 publications

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“…All of these effects could be abolished by administration of nonselective or β 1 -selective adrenergic blockade without affecting serum cytokine concentrations of TNFα or IL-10 (70). In addition, when noradrenergic neurons were depleted within the central nervous system, cellular cytokine release was affected significantly during hemorrhagic shock (71)(72)(73). Thus, hemorrhagic shock leads to vigorous increases in circulating catecholamines, which finally modulate immune cell functions via adrenergic receptors expressed on these cells.…”

Section: Foolishly Unlocking Pandora's Box?mentioning

confidence: 99%

Catecholamines—Crafty Weapons in the Inflammatory Arsenal of Immune/Inflammatory Cells or Opening Pandora’s Box?

Flierl

Rittirsch

Huber‐Lang

et al. 2008

Mol Med

160

114

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It is well established that catecholamines (CAs), which regulate immune and inflammatory responses, derive from the adrenal medulla and from presynaptic neurons. Recent studies reveal that T cells also can synthesize and release catecholamines which then can regulate T cell function. We have shown recently that macrophages and neutrophils, when stimulated, can generate and release catecholamines de novo which, then, in an autocrine/paracrine manner, regulate mediator release from these phagocytes via engagement of adrenergic receptors. Moreover, regulation of catecholamine-generating enzymes as well as degrading enzymes clearly alter the inflammatory response of phagocytes, such as the release of proinflammatory mediators. Accordingly, it appears that phagocytic cells and lymphocytes may represent a major, newly recognized source of catecholamines that regulate inflammatory responses.

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Section: Foolishly Unlocking Pandora's Box?mentioning

confidence: 99%

Catecholamines—Crafty Weapons in the Inflammatory Arsenal of Immune/Inflammatory Cells or Opening Pandora’s Box?

Flierl

Rittirsch

Huber‐Lang

et al. 2008

Mol Med

160

114

View full text Add to dashboard Cite

show abstract

“…Finally, the raised levels of Ad and CRT in the plasma are consistent with the bulk of clinical syndromes underlain by the uncoping stress syndrome parasympathetic activity that underlies this syndrome. This target was reached through the enhancement of the neural sympathetic activity that annuls both the adrenal and parasympathetic oscillations always registered in these patients [18,19,148]. With respect to the above, it is well established that parasympathetic nerves excite enterochromaffin cells.…”

Section: Carcinoid Syndromementioning

confidence: 99%

Central Nervous System Plus Autonomic Nervous System Disorders Responsible for Gastrointestinal and Pancreatobiliary Diseases

Lechín

Dijs

2008

Dig Dis Sci

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Clinical digestive disorders depend on the nonadequate coupling of functioning of the gastrointestinal tract with that of its affluent systems, namely, the pancreatic exocrine and the hepato-biliary secretions. The secretion of gastrointestinal hormones is monitored by the peripheral autonomic nervous system. However, the latter is regulated by the central nervous system (CNS) circuitry localized at the medullary pontine segment of the CNS. In turn, both parasympathetic and adrenergic medullary circuitries are regulated by the pontine A5 noradrenergic (NA) and the dorsal raphe serotonergic nuclei, respectively. DR-5HT is positively correlated with the C1-Ad medullary nuclei (responsible for adrenal gland secretion), whereas the MR-5HT nucleus is positively correlated with the A5-NA pontomedullary nucleus. The latter is responsible for neural sympathetic activity (sympathetic nerves). Both types of sympathetic activities maintain an alternation with the peripheral parasympathetic branch, which is positively correlated with the enterochromaffin cells that secrete serotonin. Serotonin displays hormonal antagonism to the circulating catecholamines.

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“…A variety of aversive stressors (e.g., electric shock) have been shown to alter NK cell function (Shavit, 1991) as well as host-resistance to NK sensitive tumors (e.g., Greenberg, Dyck, & Sandler, 1984). Other reports indicate that ehock suppresses splenic and peripheral blood lymphocyte responses to a nonspeciñc T-cell mitogen, an effect which can be blocked by arlministration of p-adrenergic antagonists (Cunnick, Lysle, Kucinski, & Rabin, 1990).…”

mentioning

confidence: 99%

Pavlovian conditioning of LPS-induced responses: Effects on corticosterone, splenic NE, and IL-2 production

Janz¹,

Green-Johnson²,

Murray³

et al. 1996

Physiology & Behavior

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Evidence that shock-induced immune suppression is mediated by adrenal hormones and peripheral β-adrenergic receptors

Cited by 151 publications

References 25 publications

Catecholamines—Crafty Weapons in the Inflammatory Arsenal of Immune/Inflammatory Cells or Opening Pandora’s Box?

Catecholamines—Crafty Weapons in the Inflammatory Arsenal of Immune/Inflammatory Cells or Opening Pandora’s Box?

Central Nervous System Plus Autonomic Nervous System Disorders Responsible for Gastrointestinal and Pancreatobiliary Diseases

Pavlovian conditioning of LPS-induced responses: Effects on corticosterone, splenic NE, and IL-2 production

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