Catecholamines and lipopolysaccharide synergistically induce the release of interleukin-6 from thymic epithelial cells

Patay, B. von; Loppnow, Harald; Feindt, Janka; Kurz, Bodo; Mentlein, Rolf

doi:10.1016/s0165-5728(98)00051-4

Cited by 44 publications

(29 citation statements)

References 31 publications

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“…In previous studies we have already shown that the basal synthesis of IL-6 in our cultures is very low and that nearly all IL-6 produced after stimulation is released into the medium [14]. We could also show that noradrenaline, adrenaline or the ß-adrenergic agonist isoproterenol dosedependently raised IL-6 synthesis to similar maximal values.…”

Section: Discussionsupporting

confidence: 72%

Effect of Transmitters and Co-Transmitters of the Sympathetic Nervous System on Interleukin-6 Synthesis in Thymic Epithelial Cells

Patay

Kurz

Mentlein³

1999

Neuroimmunomodulation

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In the thymus, sympathetic nerves run in septa in close connection to subcapsular/perivascular thymic epithelial cells (TEC). Since TEC are supposed to create a microenvironment of cytokines necessary for the development of thymocytes to T cells, we investigated the influence of sympathetic transmitters and co-transmitters on interleukin-6 (IL-6) synthesis in cultivated rat TEC that express markers of perivascular/subcapsular TEC. Noradrenaline and ATP stimulated IL-6 production in the culture supernatants 14- and 23-fold over basal values after 24 h. Co-stimulation with noradrenaline and ATP yielded an additive effect. Synthesis of IL-6 was concentration-dependent upon ATP and appeared to be mediated by P₂ purinoceptors. During 24 h stimulation with 1 mM ATP, two thirds of the ligand was degraded mainly to ADP, production of AMP and adenosine was minor or negligible. Thus, in TEC, transmitters and co-transmitters of the sympathetic nervous system have a co-stimulatory effect on synthesis of IL-6 that is an important factor for thymocyte differentiation and proliferation.

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Section: Discussionsupporting

confidence: 72%

Effect of Transmitters and Co-Transmitters of the Sympathetic Nervous System on Interleukin-6 Synthesis in Thymic Epithelial Cells

Patay

Kurz

Mentlein³

1999

Neuroimmunomodulation

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“…The addition of an α-AR agonist to unstimulated or lipopolysaccharide (LPS)-stimulated cultures of rat TEC dose-dependently increases IL-6 production, but has no effect on IL-1 production. This effect is blocked by an α-AR antagonist [57].…”

Section: Sympathetic Neurotransmission In the Thymusmentioning

confidence: 94%

“…In particular, catecholamines influence the synthesis of IL-6, which is known to affect T cell proliferation and differentiation [81]. Costimulation of cultured rat TEC with EPI, NE, or isoprenaline has an additive (tumor necrosis factor (TNF)-α) or synergistic (LPS) effect on IL-6 release mediated by β-AR that is linked to the elevation of intracellular cAMP levels [57]. A close association between mast cells and NA nerves exists in the thymus, which suggests a possible role for NE regulating mast cell function to affect thymocyte development in the thymus.…”

Section: Sympathetic Neurotransmission In the Thymusmentioning

confidence: 99%

Sympathetic modulation of immunity: Relevance to disease

Bellinger

Millar

Perez

et al. 2008

Cellular Immunology

223

185

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Optimal host defense against pathogens requires cross-talk between the nervous and immune systems. This paper reviews sympathetic-immune interaction, one major communication pathway, and its importance for health and disease. Sympathetic innervation of primary and secondary immune organs is described, as well as evidence for neurotransmission with cells of the immune system as targets. Most research thus far as focused on neural-immune modulation in secondary lymphoid organs, and have revealed complex sympathetic modulation resulting in both potentiation and inhibition of immune functions. SNS-immune interaction may enhance immune readiness during disease-or injury-induced 'fight' responses. Research also indicate that dysregulation of the SNS can significantly affect the progression of immune-mediated diseases. However, a better understanding of neural-immune interactions is needed to develop strategies for treatment of immune-mediated diseases that are designed to return homeostasis and restore normal functioning neural-immune networks.

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“…Tracing analysis indicates that thymic sympathetic outflow directly starts in neurons from the thoracic spinal cord, brainstem, caudal raphe nucleus, and hypothalamus (Trotter et al, 2007). Furthermore, the neurotransmitter norepinephrine (Singh and Owen, 1976;Felten et al, 1987;Morale et al, 1992;Tsao et al, 1996;Kurz et al, 1997;von Patay et al, 1998von Patay et al, , 1999 is found in the thymus, and thymic cells express both ␤1-and ␤2-adrenergic receptors (Morale et al, 1992;Kurz et al, 1997;von Patay et al 1999) able to modulate maturation of T precursor cells and influence the thymic microenvironment. Thus, a link between the brain and the thymus is supported at different levels.…”

Section: Autonomic Denervation Of the Gld Thymusmentioning

confidence: 99%

Autonomic Denervation of Lymphoid Organs Leads to Epigenetic Immune Atrophy in a Mouse Model of Krabbe Disease

Galbiati¹,

Basso²,

Cantuti³

et al. 2007

J. Neurosci.

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Lysosomal ␤-galactosylceramidase deficiency results in demyelination and inflammation in the nervous system causing the neurological Krabbe disease. In the Twitcher mouse model of this disease, we found that neurological symptoms parallel progressive and severe lymphopenia. Although lymphopoiesis is normal before disease onset, primary and secondary lymphoid organs progressively degenerate afterward. This occurs despite preserved erythropoiesis and leads to severe peripheral lymphopenia caused by reduced numbers of T cell precursors and mature lymphocytes. Hematopoietic cell replacement experiments support the existence of an epigenetic factor in mutant mice reconcilable with a progressive loss of autonomic axons that hampers thymic functionality. We propose that degeneration of autonomic nerves leads to the irreversible thymic atrophy and loss of immune-competence. Our study describes a new aspect of Krabbe disease, placing patients at risk of immune-related pathologies, and identifies a novel target for therapeutic interventions.

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Catecholamines and lipopolysaccharide synergistically induce the release of interleukin-6 from thymic epithelial cells

Cited by 44 publications

References 31 publications

Effect of Transmitters and Co-Transmitters of the Sympathetic Nervous System on Interleukin-6 Synthesis in Thymic Epithelial Cells

Effect of Transmitters and Co-Transmitters of the Sympathetic Nervous System on Interleukin-6 Synthesis in Thymic Epithelial Cells

Sympathetic modulation of immunity: Relevance to disease

Autonomic Denervation of Lymphoid Organs Leads to Epigenetic Immune Atrophy in a Mouse Model of Krabbe Disease

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