Central Sympathetic Modulation of Tissue Cytokine Response to Hemorrhage

Molina, Patricia E.; Abumrad, Naji N.

doi:10.1159/000026382

Cited by 7 publications

(10 citation statements)

References 41 publications

(42 reference statements)

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“…This observation contradicts earlier findings that showed decreased TNF-· production after sympathectomy [29,30]. However, numerous studies have described contradictory effects of neurotransmitters in immunomodulation [31].…”

Section: Discussioncontrasting

confidence: 91%

IL-1α and TNF-α Expression in Rat Periapical Lesions and Dental Pulp after Unilateral Sympathectomy

Bletsa

Heyeraas²,

Haug³

et al. 2004

Neuroimmunomodulation

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Objectives: Apical periodontitis is an inflammatory disease characterized by bone resorption, and sympathetic nerves are known to modulate bone resorption and bone remodeling. Higher numbers of osteoclasts and larger periapical lesions have been observed after sympathectomy in rats, but the mechanisms underlying the inhibitory effect of sympathetic nerves on osteoclasts are unknown. This study aimed to test the hypothesis that sympathetic nerves inhibit the production of the bone-resorbing pro-inflammatory cytokines IL-1α and TNF-α in rat periapical lesions. Methods: Rats were unilaterally sympathectomized and apical lesions were induced by exposing the dental pulp of molar teeth to the oral microflora. We quantified the cytokines IL-1α and TNF-α by enzyme-linked immunosorbent assay, and immunohistochemical analysis was done for qualitative localization. Pulp from intact incisor teeth was tested as a control. Results: We showed that IL-1α was increased, but not TNF-α, in the periapical lesions on the sympathectomized side. Both IL-1α and TNF-α were expressed in unexposed pulp. TNF-α was significantly decreased in the denervated incisor pulp, whereas the level of IL-1α remained unchanged. Conclusions: This study suggests that sympathetic nerves have an inhibitory effect on IL-1α in periapical lesions and a stimulatory effect on TNF-α in the intact rat pulp.

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Section: Discussioncontrasting

confidence: 91%

IL-1α and TNF-α Expression in Rat Periapical Lesions and Dental Pulp after Unilateral Sympathectomy

Bletsa

Heyeraas²,

Haug³

et al. 2004

Neuroimmunomodulation

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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

165

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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“…In addition, the depletion of noradrenergic neurons within the central nervous system affected cellular cytokine release during hemorrhagic shock [115][116][117].…”

Section: The Immunomodulatory Effect Of Peripheral Circulating Catechmentioning

confidence: 99%

Catecholamines: Physiological Immunomodulators During Health and Illness

Oberbeck

2006

CMC

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The existence of an immune-endocrine interaction has been reported and the modulatory effects of the natural occurring catecholamines epinephrine, norepinephrine and dopamine as well as of pharmaceutically generated catecholamines like dopexamine on a wide variety of immune functions were demonstrated. Furthermore, it was noticed that these effects are mediated by specific adrenergic and dopaminergic receptors expressed on the surface of immunological target cells. At first, the adrenergic immunomodulation was predominantly investigated in healthy volunteers and profound immunomodulatory effects were reported for endogenously released and exogenously administered catecholamines. To further elucidate the physiological significance of these interactions, investigators tried to reveal the importance of the catecholaminergic modulation of the immune system under pathological conditions like hemorrhagic shock and systemic inflammation, since catecholamines and adrenergic antagonists are frequently used drugs in the treatment of the critically ill. Furthermore, the interaction between catecholamines and the immune system is supposed to be an important factor in the development of autoimmune diseases and may influence their progress. In addition to the effects of peripheral circulating catecholamines, it was demonstrated that catecholamines that are released within the central nervous system may profoundly influence the activity of the peripheral immune system. Starting with a short historical overview over the immunomodulatory effects of blood catecholamines under good health conditions during critical illness and during autoimmune disease will be reviewed and the immunomodulatory effects of centrally released catecholamines will be discussed.

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Central Sympathetic Modulation of Tissue Cytokine Response to Hemorrhage

Cited by 7 publications

References 41 publications

IL-1α and TNF-α Expression in Rat Periapical Lesions and Dental Pulp after Unilateral Sympathectomy

IL-1α and TNF-α Expression in Rat Periapical Lesions and Dental Pulp after Unilateral Sympathectomy

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

Catecholamines: Physiological Immunomodulators During Health and Illness

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