Diagnostic and Therapeutic<i>Iter</i>in Chronic Urticaria Patients

Tosoni, Cinzia; Cinquini, Massimo

doi:10.1177/039463200601900203

Cited by 4 publications

(2 citation statements)

References 30 publications

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“…What triggers the expression of these genes is not clear. Some studies have data suggesting that the susceptibility to disease is genetically determined by the balance or expression of either pro-inflammatory or anti-inflammatory cytokines [30][31][32][33] .…”

Section: Discussionmentioning

confidence: 99%

Inhibitory Effect of Quercetin on Tryptase and MCP-1 Chemokine Release, and Histidine Decarboxylase mRNA Transcription by Human Mast Cell-1 Cell Line

Castellani

Kempuraj

Frydas

et al. 2006

Neuroimmunomodulation

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Mast cells are important in reactions of allergic disease and are also involved in a variety of neuroinflammatory diseases. Mast cells can be immunologically activated by IgE through their Fc receptors, as well as by neuropeptides and cytokines to secrete mediators. Here we used a human mast cell-1 (HMC-1) cell line cultured and treated with a physiological activator, anti-IgE, and a nonphysiological activator, calcium ionophore A23187, for tryptase and MCP-1 generation and transcription of histidine decarboxylase. We used quercetin, a potent antioxidant, cytoprotective and anti-inflammatory compound capable of inhibiting histamine and some cytokines released from several cell types, as an inhibitor of immunological and nonimmunological stimulus for mast cells. In this study quercetin inhibits, in a dose-response manner, tryptase and MCP-1. Moreover, using RT-PCR quercetin inhibited the transcription of histidine decarboxylase, the rate-limiting enzyme responsible for the generation of histamine from histidine, and MCP-1. Our data suggest that quercetin is an important and good candidate for reducing the release of pro-inflammatory mast cell mediators activated by physiological and nonphysiological stimulators.

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Section: Discussionmentioning

confidence: 99%

Inhibitory Effect of Quercetin on Tryptase and MCP-1 Chemokine Release, and Histidine Decarboxylase mRNA Transcription by Human Mast Cell-1 Cell Line

Castellani

Kempuraj

Frydas

et al. 2006

Neuroimmunomodulation

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show abstract

“…IFN-γ is produced by NK cells after activation from live promastigotes of L. donovani and L. aethigria in the absence of antigen-presenting cells (26). Other recently published results suggest that dendritic cells are important for NK-mediated protection and constitute the principal source of IL-12 early in leishmaniasis, as transient production of this cytokine by dendritic cells in the first 24 hours of leishmania infection appears to be the initial event that is required to trigger NK cell activation (66,67). NK cell activity also influences the viability of the intracellular protozoan parasite Neospora caninum.…”

Section: Nk Cells and Parasitesmentioning

confidence: 96%

Involvement of NK Cells against Tumors and Parasites

Papazahariadou

Athanasiadis²,

Papadopoulos

et al. 2007

Int J Biol Markers

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Expression and Secretion of CXCL8 (IL-8), Release of Tryptase and Transcription of Histidine Decarboxylase mRNA by Anti-IgE-Activated Human Umbilical Cord Blood-Derived Cultured Mast Cells

Castellani

Shaik²,

Perrella³

et al. 2007

Neuroimmunomodulation

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Activation of cytokine receptors and alterations in cytokines are thought to play important roles in neuronal dysfunction and in the pathogenesis of the nervous system diseases. CXCL8 (IL-8) is a CXC chemokine with chemotactic and inflammatory properties. Chemokines control mast cell infiltration in several inflammatory diseases, including stress and neurological dysfunctions. Using isolated human umbilical cord blood-derived cultured mast cells (HUCMC) from hematopoietic stem cells CD34+, mast cells were immunologically activated with anti-IgE at concentrations of 1, 5, 10 and 20 µg/ml leading to the dose-dependent production of IL-8 (p < 0.05). The increase in IL-8 mRNA expression was also noted when the cells were treated with anti-IgE at 10 µg/ml for 6 h. Immunologically activated HUCMC provoked the generation of tryptase in a dose- and time-dependent manner. We also found increased histidine decarboxylase (HDC) expression in activated HUCMC after 6 h of incubation, a rate-limiting enzyme responsible for the generation of histamine from histidine. Taken together, these results confirm that anti-IgE-activated mast cells release inflammatory mediators including CXCL8, a CXC chemokine which regulates several biological effects of mast cells, e.g. chemoattraction, and possibly causes cell arrest.

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Diagnostic and TherapeuticIterin Chronic Urticaria Patients

Cited by 4 publications

References 30 publications

Inhibitory Effect of Quercetin on Tryptase and MCP-1 Chemokine Release, and Histidine Decarboxylase mRNA Transcription by Human Mast Cell-1 Cell Line

Inhibitory Effect of Quercetin on Tryptase and MCP-1 Chemokine Release, and Histidine Decarboxylase mRNA Transcription by Human Mast Cell-1 Cell Line

Involvement of NK Cells against Tumors and Parasites

Expression and Secretion of CXCL8 (IL-8), Release of Tryptase and Transcription of Histidine Decarboxylase mRNA by Anti-IgE-Activated Human Umbilical Cord Blood-Derived Cultured Mast Cells

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