Stress-induced dura vascular permeability does not develop in mast cell-deficient and neurokinin-1 receptor knockout mice

Kandere‐Grzybowska, Kristiana; Gheorghe, Daniela; Priller, Josef; Esposito, Pamela; Huang, Man; Gerard, Norma P.; Theoharides, Theoharis C.

doi:10.1016/s0006-8993(03)02975-5

Cited by 63 publications

(34 citation statements)

References 49 publications

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“…Stress has also been reported to induce selective release of VEGF [78], an effect that is absent in MCdeficient mice [79]. Acute stress [80,81] and locally secreted CRH [74] activate MC [45,74], leading to neurogenic inflammation with subsequent chronic nerve sensitization [82].…”

Section: Stress Crh and Immune Cellsmentioning

confidence: 99%

Neuroendocrinology of the skin

Theoharides

Stewart

Taracanova

et al. 2016

Rev Endocr Metab Disord

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The skin is considered the mirror of the soul and is affected by neurohormonal triggers, especially stress. Hair follicles, keratinocytes, mast cells, melanocytes, and sebocytes all express sex and stress hormones implicating them in a local "hypothalamic-pituitary-adrenal axis." In particular, the peptides corticotropin-releasing hormone (CRH) and neurotensin (NT) have synergistic action stimulating mast cells and are uniquely elevated in the serum of patients with skin diseases exacerbated by stress. Addressing the neurohormonal regulation of skin function could lead to new targets for effective treatment of inflammatory skin diseases.

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Section: Stress Crh and Immune Cellsmentioning

confidence: 99%

Neuroendocrinology of the skin

Theoharides

Stewart

Taracanova

et al. 2016

Rev Endocr Metab Disord

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“…In addition, trigeminal afferents might be activated by events initiated in the brainstem. Stress can also activate meningeal plasma cells via a parasympathetic mechanism, leading to nociceptor activation [11].…”

Section: Mechanism Of Action Of Preventive Medicationsmentioning

confidence: 99%

Preventive treatment of migraine

Silberstein

2006

Trends in Pharmacological Sciences

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“…inflammation | cytokines | IL-1 | innate immunity | stress S ubstance P (SP) is an 11-amino acid peptide that mediates inflammation (1,2), partially through mast cell activation (3,4). Neuropeptides (5), especially SP, could be involved in the pathogenesis of inflammatory skin disorders, such as psoriasis (6,7), characterized by increased epidermal vascularization, keratinocyte hyperproliferation, and inflammation (8).…”

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confidence: 99%

IL-33 augments substance P–induced VEGF secretion from human mast cells and is increased in psoriatic skin

Theoharides

Zhang²,

Kempuraj³

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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The peptide substance P (SP) has been implicated in inflammatory conditions, such as psoriasis, where mast cells and VEGF are increased. A relationship between SP and VEGF has not been well studied, nor has any interaction with the proinflammatory cytokines, especially IL-33. Here we report that SP (0.1-10 μM) induces gene expression and secretion of VEGF from human LAD2 mast cells and human umbilical core blood-derived cultured mast cells (hCBMCs). This effect is significantly increased by coadministration of IL-33 (5-100 ng/mL) in both cell types. The effect of SP on VEGF release is inhibited by treatment with the NK-1 receptor antagonist 733,060. SP rapidly increases cytosolic calcium, and so does IL-33 to a smaller extent; the addition of IL-33 augments the calcium increase. SP-induced VEGF production involves calcium-dependent PKC isoforms, as well as the ERK and JNK MAPKs. Gene expression of IL-33 and histidine decarboxylase (HDC), an indicator of mast cell presence/activation, is significantly increased in affected and unaffected (at least 15 cm away from the lesion) psoriatic skin, as compared with normal control skin. Immunohistochemistry indicates that IL-33 is associated with endothelial cells in both the unaffected and affected sites, but is stronger and also associated with immune cells in the affected site. These results imply that functional interactions among SP, IL-33, and mast cells leading to VEGF release contribute to inflammatory conditions, such as the psoriasis, a nonallergic hyperproliferative skin inflammatory disorder with a neurogenic component.inflammation | cytokines | IL-1 | innate immunity | stress

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Stress-induced dura vascular permeability does not develop in mast cell-deficient and neurokinin-1 receptor knockout mice

Cited by 63 publications

References 49 publications

Neuroendocrinology of the skin

Neuroendocrinology of the skin

Preventive treatment of migraine

IL-33 augments substance P–induced VEGF secretion from human mast cells and is increased in psoriatic skin

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