Effects of Tea Infusions of Various Varieties or Different Manufacturing Types on Inhibition of Mouse Mast Cell Activation

The binding of immunoglobulin E (IgE) to high affinity IgE receptors (FcεRI) expressed on the surface of mast cells primes these cells to secrete, upon subsequent exposure to specific antigen, a panel of proinflammatory mediators, which includes cytokines that can also have immunoregulatory activities. This IgE- and antigen-specific mast cell activation and mediator production is thought to be critical to the pathogenesis of allergic disorders, such as anaphylaxis and asthma, and also contributes to host defense against parasites. We now report that exposure to IgE results in a striking (up to 32-fold) upregulation of surface expression of FcεRI on mouse mast cells in vitro or in vivo. Moreover, baseline levels of FcεRI expression on peritoneal mast cells from genetically IgE-deficient (IgE −/−) mice are dramatically reduced (by ∼83%) compared with those on cells from the corresponding normal mice. In vitro studies indicate that the IgE-dependent upregulation of mouse mast cell FcεRI expression has two components: an early cycloheximide-insensitive phase, followed by a later and more sustained component that is highly sensitive to inhibition by cycloheximide. In turn, IgE-dependent upregulation of FcεRI expression significantly enhances the ability of mouse mast cells to release serotonin, interleukin-6 (IL-6), and IL-4 in response to challenge with IgE and specific antigen. The demonstration that IgE-dependent enhancement of mast cell FcεRI expression permits mast cells to respond to antigen challenge with increased production of proinflammatory and immunoregulatory mediators provides new insights into both the pathogenesis of allergic diseases and the regulation of protective host responses to parasites.

Download Full-text

Shuang-Huang-Lian Attenuates Airway Hyperresponsiveness and Inflammation in a Shrimp Protein-Induced Murine Asthma Model

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2019/4827342 ◽

2019 ◽

Vol 2019 ◽

pp. 1-9

Author(s):

Yuan Gao ◽

Qiaoling Fei ◽

Ruijuan Qi ◽

Rui Hou ◽

Yixin Han ◽

...

Keyword(s):

Mast Cell ◽

Bronchial Asthma ◽

Airway Hyperresponsiveness ◽

Cell Activation ◽

Underlying Mechanism ◽

Lavage Fluid ◽

Mast Cell Activation ◽

Asthma Treatment ◽

Th2 Immunity ◽

Mouse Mast Cell

Shuang-Huang-Lian (SHL), an herbal formula of traditional Chinese medicine, is clinically used for bronchial asthma treatment. Our previous study found that SHL prevented basophil activation to suppress Th2 immunity and stabilized mast cells through activating its mitochondrial calcium uniporter. Sporadic clinical reports that SHL was used for the treatment of bronchial asthma can be found. Thus, in this study, we systematically investigated the effects of SHL on asthmatic responses using a shrimp protein (SP)- induced mouse model. SHL significantly inhibited airway inspiratory and expiratory resistance, and histological studies suggested it reduced thickness of airway smooth muscle and infiltration of inflammation cells. It also could alleviate eosinophilic airway inflammation (EAI), including reducing the number of eosinophils and decreasing eotaxin and eosinophil peroxidase levels in the bronchoalveolar lavage fluid (BALF). Further studies indicated that SHL suppressed SP-elevated mouse mast cell protease-1 and IgE levels, prevented Th2 differentiation in mediastinal lymph nodes, and lowered Th2 cytokine (e.g., IL-4, IL-5, and IL-13) production in BALF. In conclusion, SHL attenuates airway hyperresponsiveness and EAI mainly via the inhibition of mast cell activation and Th2 immunity, which may help to elucidate the underlying mechanism of SHL on asthma treatment and support its clinical use.

Download Full-text

Selective in vivo recruitment of the phosphatidylinositol phosphatase SHIP by phosphorylated FcγRIIB during negative regulation of IgE-dependent mouse mast cell activation

Immunology Letters ◽

10.1016/s0165-2478(96)02654-5 ◽

1996 ◽

Vol 54 (2-3) ◽

pp. 83-91 ◽

Cited By ~ 93

Author(s):

Dana C. Fong ◽

Odile Malbec ◽

Michel Arock ◽

John C. Cambier ◽

Wolf H. Fridman ◽

...

Keyword(s):

Mast Cell ◽

Cell Activation ◽

Negative Regulation ◽

Mast Cell Activation ◽

Mouse Mast Cell

Download Full-text

Trichinella spiralis Secreted Enzymes Regulate Nucleotide-Induced Mast Cell Activation and Release of Mouse Mast Cell Protease 1

Infection and Immunity ◽

10.1128/iai.00411-12 ◽

2012 ◽

Vol 80 (11) ◽

pp. 3761-3767 ◽

Cited By ~ 4

Author(s):

Holly C. Afferson ◽

Emily Eleftheriou ◽

Murray E. Selkirk ◽

Kleoniki Gounaris

Keyword(s):

Mast Cell ◽

Mast Cells ◽

Cell Activation ◽

Trichinella Spiralis ◽

Critical Role ◽

Extracellular Nucleotides ◽

Mast Cell Activation ◽

Content Type ◽

Mast Cell Protease ◽

Mouse Mast Cell

ABSTRACTExtracellular nucleotides are important triggers of innate immunity, acting on a wide variety of cells via signaling through purinergic receptors. Mucosal mast cells contribute to expulsion of a number of gastrointestinal nematode parasites, and mouse mast cell protease 1 has been shown to have a critical role in clearance ofTrichinella spiralisfrom the intestinal tract. We show here that adenosine, ADP, ATP, UDP, and UTP all stimulate calcium mobilization in bone marrow-derived mast cells with a mucosal phenotype. Secreted proteins fromT. spiralisinfective larvae inhibit nucleotide-induced mast cell activation, and that induced by ADP and UDP is specifically blocked by parasite secretory 5′-nucleotidase. Release of mouse mast cell protease 1 is stimulated by ADP and ATP. Both parasite secreted products and the 5′-nucleotidase inhibit ADP-induced release of mast cell protease, whereas that stimulated by ATP is partially inhibited by secreted products alone. This indicates that the 5′-nucleotidase contributes to but is not solely responsible for inhibition of nucleotide-mediated effects on mast cell function. Secretion of nucleotide-metabolizing enzymes by parasitic nematodes most likely evolved as a strategy for suppression of innate immune responses and is discussed in this context.

Download Full-text

TGF-β1 enhances mouse mast cell release of IL-6 and IL-13

10.1101/220665 ◽

2017 ◽

Author(s):

David O. Lyons ◽

Michele R. Plewes ◽

Nicholas A. Pullen

Keyword(s):

Mast Cell ◽

Cell Activation ◽

Potential Interaction ◽

Mast Cell Activation ◽

Hematopoietic Stem ◽

Cell Release ◽

Ige Mediated ◽

Mouse Mast Cell ◽

Positive Effect ◽

Tgf Β1

AbstractFor immune cells, TGF-β1 can enhance or repress effector functions. Here, we characterize the effects of TGF-β1 on IgE-mediated activation of primary murine mast cells derived from hematopoietic stem cells (BMMC). We also investigated potential interaction between TGF-β1 and stem-cell factor (SCF). Resting IL-6 production was increased with TGF-β1 but significance was lost following BMMC activation via IgE receptor (FcεRI) crosslinking. SCF also enhanced resting levels of IL-6, but there was no difference from control once FcεRI was engaged. SCF had no effect on IL-13 production; however, TGF-β1 treatment enhanced release of IL-13 upon FcεRI activation. Lastly, percent colocalization of SCF receptor (CD117) and FcεRI were unaffected by TGF-β1 treatment. These data reveal a novel positive effect of soluble TGF-β1 on mast cell activation.

Download Full-text

Mouse mast cell gp49B1 contains two immunoreceptor tyrosine-based inhibition motifs and suppresses mast cell activation when coligated with the high-affinity Fc receptor for IgE.

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.93.20.10809 ◽

1996 ◽

Vol 93 (20) ◽

pp. 10809-10814 ◽

Cited By ~ 116

Author(s):

H. R. Katz ◽

E. Vivier ◽

M. C. Castells ◽

M. J. McCormick ◽

J. M. Chambers ◽

...

Keyword(s):

Mast Cell ◽

Cell Activation ◽

Fc Receptor ◽

Mast Cell Activation ◽

High Affinity ◽

Mouse Mast Cell

Download Full-text

Lipid-rich enteral nutrition regulates mucosal mast cell activation via the vagal anti-inflammatory reflex

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00333.2012 ◽

2013 ◽

Vol 305 (5) ◽

pp. G383-G391 ◽

Cited By ~ 30

Author(s):

Jacco J. de Haan ◽

M'hamed Hadfoune ◽

Tim Lubbers ◽

Caroline Hodin ◽

Kaatje Lenaerts ◽

...

Keyword(s):

Mast Cell ◽

Mast Cells ◽

Cell Activation ◽

Mast Cell Activation ◽

Mucosal Mast Cell ◽

Mucosal Mast Cells ◽

Vagal Reflex ◽

Anti Inflammatory ◽

Mouse Mast Cell ◽

Stimulation Of

Nutritional stimulation of the cholecystokinin-1 receptor (CCK-1R) and nicotinic acetylcholine receptor (nAChR)-mediated vagal reflex was shown to reduce inflammation and preserve intestinal integrity. Mast cells are important early effectors of the innate immune response; therefore modulation of mucosal mast cells is a potential therapeutic target to control the acute inflammatory response in the intestine. The present study investigates intestinal mast cell responsiveness upon nutritional activation of the vagal anti-inflammatory reflex during acute inflammation. Mucosal mast cell degranulation was induced in C57/Bl6 mice by administration of Salmonella enterica LPS. Lipid-rich enteral feeding prior to LPS significantly decreased circulatory levels of mouse mast cell protease at 30 min post-LPS compared with isocaloric low-lipid nutrition or fasting. CCK-1R blockage reversed the inhibitory effects of lipid-rich feeding, whereas stimulation of the peripheral CCK-1R mimicked nutritional mast cell inhibition. The effects of lipid-rich nutrition were negated by nAChR blockers chlorisondamine and α-bungarotoxin and vagal intestinal denervation. Accordingly, release of β-hexosaminidase by MC/9 mast cells following LPS or IgE-ovalbumin complexes was dose dependently inhibited by acetylcholine and nicotine. Application of GSK1345038A, a specific agonist of the nAChR α7, in bone marrow-derived mast cells from nAChR β2−/− and wild types indicated that cholinergic inhibition of mast cells is mediated by the nAChR α7 and is independent of the nAChR β2. Together, the present study reveals mucosal mast cells as a previously unknown target of the nutritional anti-inflammatory vagal reflex.

Download Full-text