The effects of S1319, a novel marine sponge-derived β 2 -adrenoceptor agonist, on IgE-mediated activation of human cultured mast cells

Suzuki, Hajime; Ueno, Akinori; Takei, Masao; Shindo, Kazuo; Higa, Tatsuo; Fukamachi, Hiromi

doi:10.1007/s000110050563

Cited by 12 publications

(9 citation statements)

References 39 publications

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“…In contrast, cAMP could also have an inhibitory influence on mediator release. For example, a specific ␤ 2 -adrenoceptor agonist inhibited the IgE-mediated release of tryptase and TNF-␣ production in hCBMC (49). One way to possibly reconcile these data would be that cAMP could have divergent effects on different intracellular processes.…”

Section: Discussionmentioning

confidence: 99%

Human Mast Cells Express Corticotropin-Releasing Hormone (CRH) Receptors and CRH Leads to Selective Secretion of Vascular Endothelial Growth Factor

Cao

Papadopoulou

Kempuraj

et al. 2005

The Journal of Immunology

299

252

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Mast cells are critical for allergic reactions, but also for innate or acquired immunity and inflammatory conditions that worsen by stress. Corticotropin-releasing hormone (CRH), which activates the hypothalamic-pituitary-adrenal axis under stress, also has proinflammatory peripheral effects possibly through mast cells. We investigated the expression of CRH receptors and the effects of CRH in the human leukemic mast cell (HMC-1) line and human umbilical cord blood-derived mast cells. We detected mRNA for CRH-R1α, 1β, 1c, 1e, 1f isoforms, as well as CRH-R1 protein in both cell types. CRH-R2α (but not R2β or R2γ) mRNA and protein were present only in human cord blood-derived mast cells. CRH increased cAMP and induced secretion of vascular endothelial growth factor (VEGF) without tryptase, histamine, IL-6, IL-8, or TNF-α release. The effects were blocked by the CRH-R1 antagonist antalarmin, but not the CRH-R2 antagonist astressin 2B. CRH-stimulated VEGF production was mediated through activation of adenylate cyclase and increased cAMP, as evidenced by the fact that the effect of CRH was mimicked by the direct adenylate cyclase activator forskolin and the cell-permeable cAMP analog 8-bromo-cAMP, whereas it was abolished by the adenylate cyclase inhibitor SQ22536. This is the first evidence that mast cells express functional CRH receptors and that CRH can induce VEGF secretion selectively. CRH-induced mast cell-derived VEGF could, therefore, be involved in chronic inflammatory conditions associated with increased VEGF, such as arthritis or psoriasis, both of which worsen by stress.

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Section: Discussionmentioning

confidence: 99%

Human Mast Cells Express Corticotropin-Releasing Hormone (CRH) Receptors and CRH Leads to Selective Secretion of Vascular Endothelial Growth Factor

Cao

Papadopoulou

Kempuraj

et al. 2005

The Journal of Immunology

299

252

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“…As ERK1, ERK 2, JNK, and p38 have all been demonstrated to be activated in HuMCs (55,100), it is likely that the generation of prostanoids, leukotrienes, and cytokines is similarly regulated in these cells. ␤-Adrenergic agonists and phosphodiesterase inhibitors inhibit human mast cell activation via generation of cAMP and subsequent activation of PKA (101,102). One of the intracellular targets for these categories of inhibitors may be the Ras-Raf-MAPK pathway described above (101).…”

Section: Phosphatidylinositol 3-kinasementioning

confidence: 98%

FcεRI-Dependent Signaling Pathways in Human Mast Cells

Tkaczyk

Gilfillan

2001

Clinical Immunology

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“…␣-and ␤-〈Rs were detected in keratinocytes and melanocytes of human skin (219, 220, 715, 813, 814). Additionally, ␤-〈R agonists inhibited TNF-␣ release from mast cells (72) and are potent inhibitors of the IgE-mediated release of tryptase mediators from human mast cells in vitro (834). ␣-and ␤-〈Rs may also regulate important vascular responses in the skin such as vasoconstriction (215,319).…”

Section: Adrenergic Receptorsmentioning

confidence: 99%

Neuronal Control of Skin Function: The Skin as a Neuroimmunoendocrine Organ

Roosterman¹,

Goerge

Schneider

et al. 2006

Physiological Reviews

548

521

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This review focuses on the role of the peripheral nervous system in cutaneous biology and disease. During the last few years, a modern concept of an interactive network between cutaneous nerves, the neuroendocrine axis, and the immune system has been established. We learned that neurocutaneous interactions influence a variety of physiological and pathophysiological functions, including cell growth, immunity, inflammation, pruritus, and wound healing. This interaction is mediated by primary afferent as well as autonomic nerves, which release neuromediators and activate specific receptors on many target cells in the skin. A dense network of sensory nerves releases neuropeptides, thereby modulating inflammation, cell growth, and the immune responses in the skin. Neurotrophic factors, in addition to regulating nerve growth, participate in many properties of skin function. The skin expresses a variety of neurohormone receptors coupled to heterotrimeric G proteins that are tightly involved in skin homeostasis and inflammation. This neurohormone-receptor interaction is modulated by endopeptidases, which are able to terminate neuropeptide-induced inflammatory or immune responses. Neuronal proteinase-activated receptors or transient receptor potential ion channels are recently described receptors that may have been important in regulating neurogenic inflammation, pain, and pruritus. Together, a close multidirectional interaction between neuromediators, high-affinity receptors, and regulatory proteases is critically involved to maintain tissue integrity and regulate inflammatory responses in the skin. A deeper understanding of cutaneous neuroimmunoendocrinology may help to develop new strategies for the treatment of several skin diseases.

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The effects of S1319, a novel marine sponge-derived β 2 -adrenoceptor agonist, on IgE-mediated activation of human cultured mast cells

Abstract: These results indicate that S 1319 and beta-adrenoceptor agonists are potent inhibitors of the IgE-mediated release of mediators from HCMC.

Cited by 12 publications

References 39 publications

Human Mast Cells Express Corticotropin-Releasing Hormone (CRH) Receptors and CRH Leads to Selective Secretion of Vascular Endothelial Growth Factor

Human Mast Cells Express Corticotropin-Releasing Hormone (CRH) Receptors and CRH Leads to Selective Secretion of Vascular Endothelial Growth Factor

FcεRI-Dependent Signaling Pathways in Human Mast Cells

Neuronal Control of Skin Function: The Skin as a Neuroimmunoendocrine Organ

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