scholarly journals IgE-Induced Mast Cell Activation Is Suppressed by Dihydromyricetin through the Inhibition of NF-κB Signaling Pathway

Molecules ◽  
2021 ◽  
Vol 26 (13) ◽  
pp. 3877
Author(s):  
Tsong-Min Chang ◽  
Tzu-Chih Hsiao ◽  
Ting-Ya Yang ◽  
Huey-Chun Huang
Keyword(s):  
Mast Cell ◽  
Signaling Pathway ◽  
Cell Activation ◽  
Radical Scavenging ◽  
Allergic Diseases ◽  
Mast Cell Activation ◽  
Human Mast Cell ◽  
Flavonoid Compound ◽  
Enzyme Linked Immunosorbent Assay ◽  
Ku812 Cells

Mast cells play a crucial role in the pathogenesis of type 1 allergic reactions by binding to IgE and allergen complexes and initiating the degranulation process, releasing pro-inflammatory mediators. Recently, research has focused on finding a stable and effective anti-allergy compound to prevent or treat anaphylaxis. Dihydromyricetin (DHM) is a flavonoid compound with several pharmacological properties, including free radical scavenging, antithrombotic, anticancer, and anti-inflammatory activities. In this study, we investigated the anti-allergic inflammatory effects and the underlying molecular mechanism of DHM in the DNP-IgE-sensitized human mast cell line, KU812. The cytokine levels and mast cell degranulation assays were determined by enzyme-linked immunosorbent assay (ELISA). The possible mechanism of the DHM-mediated anti-allergic signaling pathway was analyzed by western blotting. It was found that treatment with DHM suppressed the levels of inflammatory cytokines TNF-α and IL-6 in DNP-IgE-sensitized KU812 cells. The anti-allergic inflammatory properties of DHM were mediated by inhibition of NF-κB activation. In addition, DHM suppressed the phosphorylation of signal transducer and activator of transcription 5 (STAT5) and mast cell-derived tryptase production. Our study shows that DHM could mitigate mast cell activation in allergic diseases.

scholarly journals Human mast cell activation through Fc receptors and Toll-like receptors

2004 ◽  
Vol 53 (3) ◽  
pp. 227-233 ◽  
Author(s):  
Yoshimichi Okayama ◽  
Shigeru Okumura ◽  
Hisashi Tomita ◽  
Hiroko Katayama ◽  
Keisuke Yuki ◽  
...  
Keyword(s):  
Mast Cell ◽  
Cell Activation ◽  
Fc Receptors ◽  
Mast Cell Activation ◽  
Human Mast Cell ◽  
Toll Like Receptors

scholarly journals The Role Played by Mitochondria in FcεRI-Dependent Mast Cell Activation

2020 ◽  
Vol 11 ◽  
Author(s):  
Maria A. Chelombitko ◽  
Boris V. Chernyak ◽  
Artem V. Fedorov ◽  
Roman A. Zinovkin ◽  
Ehud Razin ◽  
...  
Keyword(s):  
Mast Cell ◽  
Transcription Factors ◽  
Mast Cells ◽  
Cell Activation ◽  
Immunoglobulin E ◽  
Mitochondrial Dynamics ◽  
Allergic Diseases ◽  
Mast Cell Activation ◽  
Basic Knowledge ◽  
Mitochondrial Activity

Mast cells play a key role in the regulation of innate and adaptive immunity and are involved in pathogenesis of many inflammatory and allergic diseases. The most studied mechanism of mast cell activation is mediated by the interaction of antigens with immunoglobulin E (IgE) and a subsequent binding with the high-affinity receptor Fc epsilon RI (FcεRI). Increasing evidences indicated that mitochondria are actively involved in the FcεRI-dependent activation of this type of cells. Here, we discuss changes in energy metabolism and mitochondrial dynamics during IgE-antigen stimulation of mast cells. We reviewed the recent data with regards to the role played by mitochondrial membrane potential, mitochondrial calcium ions (Ca2+) influx and reactive oxygen species (ROS) in mast cell FcεRI-dependent activation. Additionally, in the present review we have discussed the crucial role played by the pyruvate dehydrogenase (PDH) complex, transcription factors signal transducer and activator of transcription 3 (STAT3) and microphthalmia-associated transcription factor (MITF) in the development and function of mast cells. These two transcription factors besides their nuclear localization were also found to translocate in to the mitochondria and functions as direct modulators of mitochondrial activity. Studying the role played by mast cell mitochondria following their activation is essential for expanding our basic knowledge about mast cell physiological functions and would help to design mitochondria-targeted anti-allergic and anti-inflammatory drugs.

scholarly journals Resveratrol inhibits IL-33–mediated mast cell activation by targeting the MK2/3–PI3K/Akt axis

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Shotaro Nakajima ◽  
Kayoko Ishimaru ◽  
Anna Kobayashi ◽  
Guannan Yu ◽  
Yuki Nakamura ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Cell Activation ◽  
Cytokine Production ◽  
Allergic Diseases ◽  
Mast Cell Activation ◽  
Akt Pathway ◽  
Mouse Lung ◽  
Mouse Bone Marrow ◽  
Interleukin 33

AbstractInterleukin-33 (IL-33)/ST2–mediated mast cell activation plays important roles in the pathophysiology of allergic diseases. Hence, pharmacologically targeting the IL-33/ST2 pathway in mast cells could help to treat such diseases. We found that resveratrol inhibits IL-33/ST2–mediated mast cell activation. Resveratrol suppressed IL-33–induced IL-6, IL-13, and TNF-α production in mouse bone marrow–derived mast cells (BMMCs), mouse fetal skin–derived mast cells, and human basophils. Resveratrol also attenuated cytokine expression induced by intranasal administration of IL-33 in mouse lung. IL-33–mediated cytokine production in mast cells requires activation of the NF-κB and MAPK p38–MAPK-activated protein kinase-2/3 (MK2/3)–PI3K/Akt pathway, and resveratrol clearly inhibited IL-33–induced activation of the MK2/3–PI3K/Akt pathway, but not the NF-κB pathway, without affecting p38 in BMMCs. Importantly, resveratrol inhibited the kinase activity of MK2, and an MK2/3 inhibitor recapitulated the suppressive effects of resveratrol. Resveratrol and an MK2/3 inhibitor also inhibited IgE-dependent degranulation and cytokine production in BMMCs, concomitant with suppression of the MK2/3–PI3K/Akt pathway. These findings indicate that resveratrol inhibits both IL-33/ST2–mediated and IgE-dependent mast cell activation principally by targeting the MK2/3–PI3K/Akt axis downstream of p38. Thus, resveratrol may have potential for the prevention and treatment of broad ranges of allergic diseases.

scholarly journals Alpha7-nicotinic acetylcholine receptors involve the imidacloprid-induced inhibition of IgE-mediated rat and human mast cell activation

RSC Advances ◽  
2017 ◽  
Vol 7 (82) ◽  
pp. 51896-51906 ◽  
Author(s):  
Linbo Shi ◽  
Huaping Xu ◽  
Yujie Wu ◽  
Xin Li ◽  
Li Zou ◽  
...  
Keyword(s):  
Mast Cell ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Cell Activation ◽  
Mast Cell Activation ◽  
Human Mast Cell ◽  
Inhibition Mechanism ◽  
Nicotinic Acetylcholine ◽  
Neonicotinoid Insecticide ◽  
Ige Mediated

Although our recent study indicated that imidacloprid, a widely used neonicotinoid insecticide, inhibited IgE-mediated mast cell activation, the inhibition mechanism still remains unclear.

scholarly journals Modulation of host defense peptide-mediated human mast cell activation by LPS

2015 ◽  
Vol 22 (1) ◽  
pp. 21-30 ◽  
Author(s):  
Kshitij Gupta ◽  
Hariharan Subramanian ◽  
Hydar Ali
Keyword(s):  
Mast Cell ◽  
Host Defense ◽  
Cell Activation ◽  
Mast Cell Activation ◽  
Human Mast Cell ◽  
Host Defense Peptide

Essential roles of sphingosine-1–phosphate receptor 2 in human mast cell activation, anaphylaxis, and pulmonary edema

2010 ◽  
Vol 188 (5) ◽  
pp. i10-i10
Author(s):  
Carole A. Oskeritzian ◽  
Megan M. Price ◽  
Nitai C. Hait ◽  
Dmitri Kapitonov ◽  
Yves T. Falanga ◽  
...  
Keyword(s):  
Mast Cell ◽  
Pulmonary Edema ◽  
Cell Activation ◽  
Mast Cell Activation ◽  
Human Mast Cell ◽  
Sphingosine 1 Phosphate

scholarly journals Direct Inhibition of the Allergic Effector Response by Raw Cow’s Milk—An Extensive In Vitro Assessment

Cells ◽  
2020 ◽  
Vol 9 (5) ◽  
pp. 1258
Author(s):  
Suzanne Abbring ◽  
Bart R. J. Blokhuis ◽  
Julie L. Miltenburg ◽  
Kiri G. J. Romano Olmedo ◽  
Johan Garssen ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Cell Activation ◽  
Allergic Diseases ◽  
Raw Milk ◽  
Mast Cell Activation ◽  
Cow’S Milk ◽  
Cow's Milk ◽  
Ige Mediated ◽  
Raw Cow’S Milk

The mechanisms underlying the allergy-protective effects of raw cow’s milk are poorly understood. The current focus is mainly on the modulation of T cell responses. In the present study, we investigated whether raw cow’s milk can also directly inhibit mast cells, the key effector cells in IgE-mediated allergic responses. Primary murine bone marrow-derived mast cells (BMMC) and peritoneal mast cells (PMC), were incubated with raw milk, heated raw milk, or shop milk, prior to IgE-mediated activation. The effects on mast cell activation and underlying signaling events were assessed. Raw milk was furthermore fractionated based on molecular size and obtained fractions were tested for their capacity to reduce IgE-mediated mast cell activation. Coincubation of BMMC and PMC with raw milk prior to activation reduced β-hexosaminidase release and IL-6 and IL-13 production, while heated raw milk or shop milk had no effect. The reduced mast cell activation coincided with a reduced intracellular calcium influx. In addition, SYK and ERK phosphorylation levels, both downstream signaling events of the FcεRI, were lower in raw milk-treated BMMC compared to control BMMC, although differences did not reach full significance. Raw milk-treated BMMC furthermore retained membrane-bound IgE expression after allergen stimulation. Raw milk fractionation showed that the heat-sensitive raw milk components responsible for the reduced mast cell activation are likely to have a molecular weight of > 37 kDa. The present study demonstrates that raw cow’s milk can also directly affect mast cell activation. These results extend the current knowledge on mechanisms via which raw cow’s milk prevents allergic diseases, which is crucial for the development of new, microbiologically safe, nutritional strategies to reduce allergic diseases.

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