scholarly journals Characterization of Functional Vanilloid Receptors Expressed by Mast Cells

Blood ◽  
1998 ◽  
Vol 91 (4) ◽  
pp. 1332-1340 ◽  
Author(s):  
Tamás Bı́ró ◽  
Marcus Maurer ◽  
Shayan Modarres ◽  
Nancy E. Lewin ◽  
Chaya Brodie ◽  
...  
Keyword(s):  
Mast Cells ◽  
Ruthenium Red ◽  
Dorsal Root Ganglion Neurons ◽  
Interleukin 4 ◽  
Vanilloid Receptors ◽  
45Ca Uptake ◽  
Ganglion Neurons ◽  
Type Receptor

Abstract Capsaicin and its ultrapotent analog resiniferatoxin (RTX) act through specific vanilloid receptors on sensory neurons. The C-type receptor is coupled to 45Ca uptake, whereas the R-type is detectable by [3H]RTX binding. We describe here specific vanilloid responses in murine mast cells (MCs). In the MC lines and in bone marrow-derived mast cells, capsaicin and RTX induced45Ca uptake similarly to that observed for cultured rat dorsal root ganglion neurons (DRGs). This response was antagonized by the antagonists capsazepine and ruthenium red. As in DRGs, pretreatment of MCs with capsaicin or RTX induced desensitization to subsequent stimulation of 45Ca uptake. The potency for desensitization by RTX in the MCs corresponded to that for 45Ca uptake, whereas in DRGs it occurred at significantly lower concentrations corresponding to that for the high-affinity [3H]RTX binding site. Consistent with this difference, in MCs we were unable to detect [3H]RTX binding. Vanilloids were noncytotoxic to the MCs, in contrast to the DRGs. Although vanilloids did not cause degranulation in MCs, in the P815 clone capsaicin evoked selective interleukin-4 release. We conclude that certain MCs possess vanilloid receptors, but only the C-type that functions as a channel. Our finding that MCs can respond directly to capsaicin necessitates a reevaluation of the in vivo pathway of inflammation in response to vanilloids.

scholarly journals Temporal mechanically-induced signaling events in bone and dorsal root ganglion neurons after in vivo bone loading

PLoS ONE ◽  
2018 ◽  
Vol 13 (2) ◽  
pp. e0192760
Author(s):  
Jason A. Bleedorn ◽  
Troy A. Hornberger ◽  
Craig A. Goodman ◽  
Zhengling Hao ◽  
Susannah J. Sample ◽  
...  
Keyword(s):  
Dorsal Root Ganglion ◽  
Dorsal Root ◽  
Dorsal Root Ganglion Neurons ◽  
Signaling Events ◽  
Bone Loading ◽  
Ganglion Neurons

scholarly journals Analgesic Effects of Cnidium officinale Extracts on Postoperative, Neuropathic, and Menopausal Pain in Rat Models

2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
Eun Yeong Lim ◽  
Jae Goo Kim ◽  
Jaekwang Lee ◽  
Changho Lee ◽  
Jaewon Shim ◽  
...  
Keyword(s):  
Ferulic Acid ◽  
Dorsal Root Ganglion Neurons ◽  
Great Efficacy ◽  
Withdrawal Threshold ◽  
Analgesic Effects ◽  
Pain Models ◽  
Cnidium Officinale ◽  
Model Treatment ◽  
Ganglion Neurons

Cnidium officinale, widely cultivated in East Asia, has been reported to exhibit pharmacological efficacy in various disorders. However, little has been reported on its role as a pain killer. In this study, we reveal that the C. officinale extract (COE) has great efficacy as a novel analgesic in various in vivo pain models. Administration of COE attenuated hypersensitivity in all postoperative, neuropathic, and menopausal pain models. Decreased hyperalgesia was confirmed by a mechanical withdrawal threshold assay and ultrasonic vocalization call analysis. In addition, application of COE inhibited the induction of the proinflammatory cytokines and calpain-3 on dorsal root ganglion neurons in a spared nerve injury rat model. Treatment with ferulic acid, which was identified as one of the components of COE by HPLC analysis, alleviated nociceptive behaviors. Our findings suggest that ferulic acid is an active compound from COE, and COE is a potential phytomedical source for pain relief by inhibiting the process of inflammation.

scholarly journals Interleukin-4 (IL-4) enhances and soluble interleukin-4 receptor (sIL-4R) inhibits histamine release from peripheral blood basophils and mast cellsin vitroandin vivo

1997 ◽  
Vol 6 (2) ◽  
pp. 111-118 ◽  
Author(s):  
B. Niggemann ◽  
T. Zuberbier ◽  
U. Herz ◽  
K. Enssle ◽  
U. Wahn ◽  
...  
Keyword(s):  
Mast Cells ◽  
Histamine Release ◽  
Peripheral Blood ◽  
Specific Ige ◽  
Interleukin 4 ◽  
Effector Cells ◽  
Antibody Titres ◽  
Interleukin 4 Receptor

The aim of the study was to analyse the effect of interleukin-4 (IL-4) on allergen and anti-IgE mediated histamine release from basophils and human skin mast cells and to assess whether soluble recombinant interleukin-4 receptor (sIL4R) can inhibit these effects. Anti-IgE stimulated histamine release from peripheral blood basophils and mast cells of atopic donors was enhanced after preincubation with IL-4, whereas after preincubation with sIL-4R it was inhibited. These effects were even more pronounced when samples were stimulated with a clinically relevant allergen. In IL-4 preincubated skin mast cells, there was a similar enhancement of anti-IgE stimulated histamine release, which could again be inhibited by sIL-4R. The effects of IL-4 and sIL4R were dose- and time-dependent. Mice sensitized to ovalbumin and treated with soluble recombinant murine sIL-4R showed significantly reduced immediate-type cutaneous hypersensitivity responses compared with untreated mice. Thesein vivoeffects were IgE independent, since there were no significant differences in total and allergen specific IgE/IgG1 antibody titres between treated and untreated mice. This indicates that IL4 exerts priming effects on histamine release by effector cells of the allergic response and that these effects are potently antagonized by soluble IL-4R bothin vitroandin vivo.

scholarly journals High-resolution tracking of cell division demonstrates differential effects of TH1 and TH2 cytokines on SCF-dependent human mast cell production in vitro:correlation with apoptosis and Kit expression

Blood ◽  
2005 ◽  
Vol 105 (2) ◽  
pp. 592-599 ◽  
Author(s):  
Marianna Kulka ◽  
Dean D. Metcalfe
Keyword(s):  
Mast Cell ◽  
Cell Division ◽  
Mast Cells ◽  
Cell Number ◽  
Interleukin 4 ◽  
Human Mast Cell ◽  
T Helper 1 ◽  
Cell Production ◽  
Ifn Γ

Abstract T-helper 1 (TH1) (interferon-γ [IFN-γ]) and TH2 (interleukin-4 [IL-4] and IL-5) cytokines have been variably reported to alter human mast cell numbers in complex culture systems. The effects of these cytokines on the kinetics of cell division and cell death are unknown, and their effect on mast cell behavior is relevant to anticipate the consequences of in vivo strategies that alter cytokine levels. To determine the effect of these cytokines on stem cell factor (SCF)–dependent human mast cell production, we used highresolution tracking of cell division and correlated the results with cell apoptosis, expression of Kit, and mast cell degranulation. When IFN-γ, IL-5, or IL-4 was administered over 8 weeks, we found each cytokine decreased the mast number through a different mechanism. IFN-γ inhibited early progenitor cell division, IL-4 down-regulated early Kit expression, and IL-5 blocked later cell division. Further, IL-4 and IFN-γ had the greatest suppressive effect on degranulation and FcϵRI expression. When these cytokines were administered to mature mast cells, IFN-γ and IL-5 had no effect on degranulation and cell division, but IL-4 induced division and potentiated FcϵRI-mediated degranulation. Thus, exposure of human mast cells to IL-4, IL-5, and IFN-γ during growth and differentiation generally down-regulated mast cell number and function, whereas IL-4 increased mature mast cell division and degranulation.

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