Substance P can stimulate prostaglandin D2 and leukotriene C4 generation without granule exocytosis in murine mast cells

Karimi, Khalil; Kool, Mirjam; Nijkamp, Frans P.; Redegeld, Frank A.

doi:10.1016/j.ejphar.2004.03.003

Cited by 20 publications

(20 citation statements)

References 41 publications

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“…SP induces LTC 4 release from murine mast cells [26], but RBL-2H3 cells in our study did not. The discrepancy may be due to the different sources of the mast cells, similar to the controversy of histamine release [24,25].…”

Section: Discussioncontrasting

confidence: 42%

Enhancement of the release of inflammatory mediators by substance P in rat basophilic leukemia RBL-2H3 cells

Liao

Hou

Wang³

et al. 2006

J Biomed Sci

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SummarySubstance P (SP), a neurotransmitter, may play an important role in neurogenic inflammation. Ginseng has been used extensively in traditional medicine; however, few studies were focused on their anti-allergic effect. Therefore, the effect and mechanism of ginsenoside Rb1 on the SP enhancement of allergic mediators were explored. In this study, SP and dinitrophenyl-bovine serum albumin (DNP-BSA) were used to activate rat basophilic leukemia (RBL)-2H3 cells. The cultured supernatants were assayed for histamine, leukotriene C 4 (LTC 4 ) and interleulin-4 (IL-4) production. The mitogen-activated protein kinases (MAPKs) signaling pathway was determined by Western blotting analysis. We found that IgE/DNP-BSA, SP, ginsenoside Rb1, or MAPK specific inhibitors had no effect on cell viability and cytotoxicity. SP (30 lM) alone, did not induce histamine and LTC 4 release, but it enhanced allergen-induced histamine and LTC 4 release. In addition, SP significantly induced and enhanced allergen-activated IL-4. Ginsenoside Rb1 dosedependently inhibited these effects. SP enhanced the allergen-activated ERK pathway in RBL-2H3 cells, and Rb1 effectively inhibited the ERK pathway activation. Although MAPK specific inhibitors suppressed LTC 4 and IL-4, only U0126 inhibited the SP enhanced histamine release. These results demonstrate that Rb1 dose-dependently inhibited SP enhanced allergen-induced mediator release and its mechanism was through the inhibition of the ERK pathway.

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Section: Discussioncontrasting

confidence: 42%

Enhancement of the release of inflammatory mediators by substance P in rat basophilic leukemia RBL-2H3 cells

Liao

Hou

Wang³

et al. 2006

J Biomed Sci

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“…The NK-1 receptor is also expressed on rat basophilic leukemia cells (47), activation of which by neurites occurred via SP (48). In contrast, murine bone marrow-derived mast cells did not release histamine in response to SP, but they did produce prostaglandin D 2 and leukotrience C 4 (49). Degranulation, as compared with de novo synthesis of selected mediators, may involve direct activation of G proteins (50,51), as shown for SP (52) and the bee venom peptide mastoparan (53,54).…”

Section: Discussionmentioning

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.

298

272

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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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“…SOM is known to modulate lymphocyte proliferation [76], whereas CGRP increases chemotaxis, promotes adhesion of lymphocytes [77], and inhibits Th1 cytokine synthesis, causing a disbalance of Th1/Th2-derived cytokines in favor of Th2 [78]. For mast cells, it has been demonstrated that SP cause activation and promote the release of histamine [79], leukotriene C4 [80], IL-6 [81], prostaglandin D2 [80], and TNF-α [81]. In contrast, neurotrophin-modulated neuropeptide release may induce eosinophilic airway inflammation by direct binding to eosinophils or indirectly by exerting various effects on mast cells and T lymphocytes.…”

Section: Sensory Neurons: Modulation Of Neuropeptide Synthesismentioning

confidence: 99%

Neurotrophin effects on eosinophils in allergic inflammation

Nassenstein

Braun

Nockher

et al. 2005

Curr Allergy Asthma Rep

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Elevated neurotrophin concentrations have been shown in nasal and bronchoalveolar lavage fluids as well as in the sera of patients with allergic rhinitis and asthma. Concentration of nerve growth factor correlated with disease severity, bronchial hyperreactivity, and levels of mediators released from eosinophils. Due to the release of cationic proteins, oxygen species, and cytokines after degranulation, eosinophils contribute to tissue damage and can influence airway hyperresponsiveness in asthma. It has been hypothesized that neurotrophins may be involved in the development of eosinophilia and in activation of these cells. The aim of this review is to elucidate the direct and indirect mechanisms of neurotrophins contributing to eosinophilia in allergic diseases.

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Substance P can stimulate prostaglandin D2 and leukotriene C4 generation without granule exocytosis in murine mast cells

Cited by 20 publications

References 41 publications

Enhancement of the release of inflammatory mediators by substance P in rat basophilic leukemia RBL-2H3 cells

Enhancement of the release of inflammatory mediators by substance P in rat basophilic leukemia RBL-2H3 cells

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

Neurotrophin effects on eosinophils in allergic inflammation

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