Clinacanthus nutans Aqueous Extract But Not Ethanolic Extract Inhibits the Release of Preformed Mediators in In Vitro Model of IgE-Mediated Mast Cell Degranulation

2017 ◽  
Vol 1 (2) ◽  
Author(s):  
Audrey Siew Foong Kow ◽  
Lai Yen Fong ◽  
Leng Wei Khoo ◽  
Ji Wei Tan ◽  
Khozirah Shaari ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Aqueous Extract ◽  
Inflammatory Mediators ◽  
Scientific Evidence ◽  
Ethanolic Extract ◽  
Mast Cell Degranulation ◽  
Traditional Use ◽  
Medicinal Uses

C. nutans (Burm. f.) Lindau is a shrub that is commonly found in South East Asia, particularly in Malaysia, Thailand and Indonesia. This plant has diverse and potential medicinal uses in traditional herbal medicine for treating many diseases which include skin rashes. Skin rash is one of the symptoms that primarily occur in people with allergies. Till date, there has been no scientific evidence to support this traditional use of C. nutans as well as its potential of possessing anti-allergic properties. IgE and mast cells play an important role in the pathogenesis of allergy. Upon cross-linking of allergen to IgE antibodies bound to FcεRI on mast cells, pro-inflammatory mediators will be released as a result of degranulation. The release of pro-inflammatory mediators by mast cells activated by allergen in the skin causes large, itchy, red swellings of the skin. This study aimed to identify the most active C. nutans extract in inhibiting in vitro IgE-mast cell degranulation. Rat basophilic leukaemic cells (RBL-2H3) were pre-sensitised with IgE, pre-treated with C. nutans ethanolic (100%, 70% and 50%) or aqueous extracts and challenged with dinitrophenyl-bovine serum albumin (DNP-BSA) accordingly to analyse the release of β-hexosaminidase, histamine, interleukin (IL)-4 and tumour necrosis factor (TNF)-α. It was found that C. nutans aqueous extract was the most active extract compared to the ethanolic extracts as it was able to inhibit the release of β-hexosaminidase and histamine at concentrations of 5 mg/ml and above.

In-vitro and in-vivo Evaluation of Anti-asthmatic Activity of Eugenia jambolana bark

2021 ◽  
pp. 3337-3342
Author(s):  
Bhong Prabha N. ◽  
Naikawade Nilofar. S. ◽  
Mali Pratibha. R. ◽  
Bindu Madhavi. S.
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Animal Models ◽  
Aqueous Extract ◽  
Guinea Pigs ◽  
Bark Extract ◽  
Eugenia Jambolana ◽  
In Vivo Animal Models

Objectives: The present study designed to evaluate the Antiasthmatic activity of aqueous extract of bark of Eugenia Jambolana (AEEJ) on in vitro and in vivo animal models. Materials and methods: Different in vitro and in vivo animal models was used to study the anti asthmatic activity as isolated goat tracheal chain preparation, Acetylcholine and Histamine induced bronconstriction in guinea pigs, effect of drug extract on histamine release from mast cell was checked by clonidine-induced mast cell degranulation, and milk-induced eosinophilia and leukocytosis. Results: In-vitro study on goat tracheal chain preparation revealed that aqueous extract of Eugenia jambolana (AEEJ)bark exerted antagonistic effect on the histamine induced contraction. (P<0.05) The guinea pigs when exposed to 0.2% histamine aerosol showed signs of progressive dyspnoea leading to convulsions. AEEJ significantly prolonged the latent period of convulsions (PCT) as compared to control following the exposure of histamine (0.2%) aerosol (P<0.01). The observation of present study indicates aqueous extract of Eugenia jambolana shows significant inhibition of milk induced eosinophilia and leukocytosis. Group of animals pretreated with aqueous Eugenia jambolana bark extract showed significant reduction in degranulation of mast cells when challenged with clonidine. The prevention of degranulation process by the aqueous Eugenia jambolana bark extract (P<0.01) indicates a possible stabilizing effect on the mast cells, indicating mast cell stabilizing activity. Conclusions: Thus, AEEJ showed antihistaminic, mast cell stabilizing and protective in guinea pigs against histamine induced PCD, reduced eosinophilia and leukocytosis and hence possesses potential role in the treatment of asthma.

Dural mast cell degranulation is a putative mechanism for headache induced by PACAP-38

Cephalalgia ◽  
2012 ◽  
Vol 32 (4) ◽  
pp. 337-345 ◽  
Author(s):  
Michael Baun ◽  
Martin Holst Friborg Pedersen ◽  
Jes Olesen ◽  
Inger Jansen-Olesen
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Adenylate Cyclase ◽  
Phospholipase C ◽  
Dura Mater ◽  
Mast Cell Degranulation ◽  
Peritoneal Mast Cell ◽  
Selective Blockade ◽  
Peritoneal Mast Cells

Background: Pituitary adenylate cyclase activating peptide-38 (PACAP-38) has been shown to induce migraine in migraineurs, whereas the related peptide vasoactive intestinal peptide (VIP) does not. In the present study we examine the hypothesis that PACAP-38 and its truncated version PACAP-27 but not VIP cause degranulation of mast cells in peritoneum and in dura mater. Methods: The degranulatory effects of PACAP-38, PACAP-27 and VIP were investigated by measuring the amount of N-acetyl-β-hexosaminidase released from isolated peritoneal mast cells and from dura mater attached to the skull of the rat in vitro. In peritoneal mast cells N-truncated fragments of PACAP-38 (PACAP(6–38), PACAP(16–38) and PACAP(28–38)) were also studied. To investigate transduction pathways involved in mast cell degranulation induced by PACAP-38, PACAP-27 and VIP, the phospholipase C inhibitor U-73122 and the adenylate cyclase inhibitor SQ 22536 were used. Results: The peptides induced degranulation of isolated peritoneal mast cells of the rat with the following order of potency: PACAP-38 = PACAP(6–38) = PACAP(16–38) » PACAP-27 = VIP = PACAP(28–38). In the dura mater we found that 10−5 M PACAP-38 was significantly more potent in inducing mast cell degranulation than the same concentration of PACAP-27 or VIP. Inhibition of intracellular mechanisms demonstrated that PACAP-38-induced degranulation is mediated by the phospholipase C pathway. Selective blockade of the PAC1 receptor did not attenuate degranulation. Conclusion: These findings correlate with clinical studies and support the hypothesis that mast cell degranulation is involved in PACAP-induced migraine. PACAP-38 has a much stronger degranulatory effect on rat peritoneal and dural mast cells than VIP and PACAP-27. The difference in potency between PACAP-38- and PACAP-27/VIP-induced peritoneal mast cell degranulation is probably not related to the PAC1 receptor but is caused by a difference in efficacy on phospholipase C.

scholarly journals Glaucocalyxin A Attenuates Allergic Responses by Inhibiting Mast Cell Degranulation through p38MAPK/NrF2/HO-1 and HMGB1/TLR4/NF-κB Signaling Pathways

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Yihua Piao ◽  
Jingzhi Jiang ◽  
Zhiguang Wang ◽  
Chongyang Wang ◽  
Shan Jin ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Signaling Pathway ◽  
Nuclear Translocation ◽  
Calcium Influx ◽  
Mast Cell Degranulation ◽  
Therapeutic Drug ◽  
High Mobility Group Protein

Glaucocalyxin A (GLA) has various pharmacological effects like antioxidation, immune regulation, and antiatherosclerosis. Here, in this study, the effect and mechanism of GLA on mast cell degranulation were studied. The results of the anti-DNP IgE-mediated passive cutaneous anaphylaxis (PCA) showed that GLA dramatically inhibited PCA in vivo, as evidenced by reduced Evans blue extravasation and decreased ear thickness. In addition, GLA significantly reduced the release of histamine and β-hexosaminidase, calcium influx, cytokine (IL-4, TNF-α, IL-1β, IL-13, and IL-8) production in the RBL-2H3 (rat basophilic leukemia cells), and RPMCs (peritoneal mast cells) in vitro. Moreover, we further investigated the regulatory mechanism of GLA on antigen-induced mast cells by Western blot, which showed that GLA inhibited FcεRI-mediated signal transduction and invalidated the phosphorylation of Syk, Fyn, Lyn, Gab2, and PLC-γ1. In addition, GLA inhibited the recombinant mouse high mobility group protein B1- (HMGB1-) induced mast cell degranulation through limiting nuclear translocation of NF-κBp65. Treatment of mast cells with siRNA-HMGB1 significantly inhibited HMGB1 levels, as well as MyD88 and TLR4, decreased intracellular calcium levels, and suppressed the release of β-hexosaminidase. Meanwhile, GLA increased NrF2 and HO-1 levels by activating p38MAPK phosphorylation. Consequently, these data suggest that GLA regulates the NrF2/HO-1 signaling pathway through p38MAPK phosphorylation and inhibits HMGB1/TLR4/NF-κB signaling pathway to reduce mast cell degranulation and allergic inflammation. Our findings could be used as a promising therapeutic drug against allergic inflammatory disease.

scholarly journals Denatonium Benzoate Exposure Promotes IgE-Mediated Mast Cell Degranulation and Allergy By Upregulating FcεRIα Expression

2021 ◽  
Author(s):  
Huaping Xu ◽  
Xiaoyun Shi ◽  
Mengting Xie ◽  
Shiyu Xiao ◽  
Xin Li ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Cell Surface ◽  
Surface Expression ◽  
Specific Ige ◽  
Mast Cell Degranulation ◽  
Cell Surface Expression ◽  
Denatonium Benzoate ◽  
Ige Mediated

Abstract Background: Denatonium benzoate (DB), one of the bitterest compounds known to man, is currently added to a wide range of products and is also used for alcohol denaturation. Some reports demonstrated that asthmatic symptoms are associated with DB exposure but the possible links between DB and IgE-mediated allergy susceptibility have not been examined to date. We investigated the effects of DB on IgE-mediated mast cell degranulation in vitro and in the ovalbumin (OVA)-induced mouse model of allergy.Methods: DB treatments were given to RBL-2H3 IgE-sensitized rat mast cell/basophil cells and KU812 human basophilic cells together with OVA-induced allergic BALB/c mice. Allergic mediator release, Ca2+ influx and OVA-specific IgE anaphylactic shock symptoms were measured along with the cell-surface expression of the α-subunit of high-affinity IgE receptor FcεRI on mast cells.Results: DB increases β-hexosaminidase (β-hex) release and Ca2+ mobilization in IgE-mediated activated RBL-2H3 and KU812 cells, and enhanced the cell-surface expression of FcεRIα. DB also promoted the severity of OVA-induced anaphylactic and diarrheic symptoms which was accompanied by mucus thickness in jejunum and the levels of β-hex, histamine and OVA-specific IgE in allergy mice, as well as the levels of FcεRIα mRNA and the FcεRIα proteinin isolated mucosal mast cells. Conclusions: DB treatments can promote the IgE-mediated mast cell degranulation in vitro and OVA-induced allergic susceptibility in mice by upregulating mast-cell-surface FcεR1α expression, providing evidence for DB exposure in promoting allergy susceptibility.

Mucosal mast cells and developmental changes in gastric absorption

1995 ◽  
Vol 268 (1) ◽  
pp. G121-G127 ◽  
Author(s):  
A. G. Catto-Smith ◽  
J. L. Ripper
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Short Circuit ◽  
Mast Cell Degranulation ◽  
Mucosal Mast Cell ◽  
Sprague Dawley ◽  
Mucosal Permeability ◽  
Mucosal Mast Cells ◽  
Gastric Mucosal Mast Cell

We aimed to establish whether gastric mucosal mast cells undergo degranulation during normal postnatal development and to correlate this with gastric electrical parameters, paracellular permeability, and macromolecular absorption. Sprague-Dawley rats were studied between 10 and 30 days after birth. Gastric mucosal mast cell degranulation occurred and was maximal on days 15 and 17, measured by histology and gastric and serum levels of rat mast cell protease II. Short-circuit current, transepithelial conductance, and permeability of voltage-clamped glandular stomach were elevated in younger animals, falling with age except for a transient but significant increase in conductance and permeability at 17 days, closely correlated with maximal mast cell degranulation. Macromolecular uptake was significantly increased in animals aged 10-15 days. Concanavalin A and antigen-induced mast cell degranulation increased conductance and permeability in vitro in younger animals. We conclude that 1) gastric mucosal mast cells degranulate during development, 2) the neonatal stomach has increased permeability and uptake of macromolecules, and 3) gastric mucosal mast cell degranulation during development may affect mucosal permeability.

Histamine, mast cells and ovarian function

1989 ◽  
Vol 120 (3) ◽  
pp. 363-371 ◽  
Author(s):  
A. Krishna ◽  
K. Beesley ◽  
P. F. Terranova
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Ovarian Function ◽  
Cell Types ◽  
Mast Cell Degranulation ◽  
Future Research ◽  
Corpora Lutea ◽  
Theca Externa

ABSTRACT Mast cells, endothelial cells, basophils and platelets are potential sources of histamine in the ovary. Little is known about the role of the latter three cell types in ovarian function. Several studies have revealed changes in the number and degranulation (release of histamine) of mast cells in the ovary during the cycle. Mast cells degranulate on pro-oestrus in the rodent ovary, and mast cells numbers increase in the theca externa of the dominant follicle in the bovine ovary. In rodents, mast cells are limited to the ovarian hilum and are not observed in follicles, corpora lutea and interstitium; this contrasts with larger species such as man, cows and monkeys where mast cells are observed throughout the ovary. Evidence is accumulating that mast cell degranulation in the ovary may be regulated by neuronal input. Neurones have been shown to have close morphological relationships with mast cells in the ovary. Histamine participates in regulating capillary permeability and blood flow in the ovary. These actions are induced by injections of LH, yet the mechanism by which LH induces mast cell degranulation is unknown. Histamine stimulates ovarian contractility, ovulation and follicular progesterone secretion in vitro. Whether these actions of histamine occur in vivo are currently unknown. This review gives a chronological description of the discoveries of the effects of histamine on ovarian function and makes suggestions for future research in this area. Journal of Endocrinology (1989) 120, 363–371

Development of hematopoietic cells lacking transcription factor GATA-1

Development ◽  
1995 ◽  
Vol 121 (1) ◽  
pp. 163-172 ◽  
Author(s):  
L. Pevny ◽  
C.S. Lin ◽  
V. D'Agati ◽  
M.C. Simon ◽  
S.H. Orkin ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Mast Cell ◽  
Cell Differentiation ◽  
Mast Cells ◽  
Blood Cell ◽  
Embryonic Stem ◽  
Sequence Motif ◽  
Erythroid Cells ◽  
Gata Factor

GATA-1 is a zinc-finger transcription factor believed to play an important role in gene regulation during the development of erythroid cells, megakaryocytes and mast cells. Other members of the GATA family, which can bind to the same DNA sequence motif, are co-expressed in several of these hemopoietic lineages, raising the possibility of overlap in function. To examine the specific roles of GATA-1 in hematopoietic cell differentiation, we have tested the ability of embryonic stem cells, carrying a targeted mutation in the X-linked GATA-1 gene, to contribute to various blood cell types when used to produce chimeric embryos or mice. Previously, we reported that GATA-1- mutant cells failed to contribute to the mature red blood cell population, indicating a requirement for this factor at some point in the erythroid lineage (L. Pevny et al., (1991) Nature 349, 257–260). In this study, we have used in vitro colony assays to identify the stage at which mutant erythroid cells are affected, and to examine the requirement for GATA-1 in other lineages. We found that the development of erythroid progenitors in embryonic yolk sacs was unaffected by the mutation, but that the cells failed to mature beyond the proerythroblast stage, an early point in terminal differentiation. GATA-1- colonies contained phenotypically normal macrophages, neutrophils and megakaryocytes, indicating that GATA-1 is not required for the in vitro differentiation of cells in these lineages. GATA-1- megakaryocytes were abnormally abundant in chimeric fetal livers, suggesting an alteration in the kinetics of their formation or turnover. The lack of a block in terminal megakaryocyte differentiation was shown by the in vivo production of platelets expressing the ES cell-derived GPI-1C isozyme. The role of GATA-1 in mast cell differentiation was examined by the isolation of clonal mast cell cultures from chimeric fetal livers. Mutant and wild-type mast cells displayed similar growth and histochemical staining properties after culture under conditions that promote the differentiation of cells resembling mucosal or serosal mast cells. Thus, the mast and megakaryocyte lineages, in which GATA-1 and GATA-2 are co-expressed, can complete their maturation in the absence of GATA-1, while erythroid cells, in which GATA-1 is the predominant GATA factor, are blocked at a relatively early stage of maturation.

scholarly journals Mast cell activation is not required for induction of airway hyperresponsiveness by ozone in mice

1999 ◽  
Vol 86 (1) ◽  
pp. 202-210 ◽  
Author(s):  
N. Noviski ◽  
J. P. Brewer ◽  
W. A. Skornik ◽  
S. J. Galli ◽  
J. M. Drazen ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Airway Hyperresponsiveness ◽  
Essential Role ◽  
Cell Activation ◽  
Mast Cell Degranulation ◽  
Mast Cell Activation ◽  
Polymorphonuclear Cell ◽  
Pulmonary Parenchyma

Exposure to ambient ozone (O3) is associated with increased exacerbations of asthma. We sought to determine whether mast cell degranulation is induced by in vivo exposure to O3in mice and whether mast cells play an essential role in the development of pulmonary pathophysiological alterations induced by O3. For this we exposed mast cell-deficient WBB6F1- kitW/ kitW-v( kitW/ kitW-v) mice and the congenic normal WBB6F1(+/+) mice to air or to 1 or 3 parts/million O3for 4 h and studied them at different intervals from 4 to 72 h later. We found evidence of O3-induced cutaneous, as well as bronchial, mast cell degranulation. Polymorphonuclear cell influx into the pulmonary parenchyma was observed after exposure to 1 part/milllion O3only in mice that possessed mast cells. Airway hyperresponsiveness to intravenous methacholine measured in vivo under pentobarbital anesthesia was observed in both kitW/ kitW-vand +/+ mice after exposure to O3. Thus, although mast cells are activated in vivo by O3and participate in O3-induced polymorphonuclear cell infiltration into the pulmonary parenchyma, they do not participate detectably in the development of O3-induced airway hyperresponsiveness in mice.

Sign in / Sign up

Export Citation Format

Share Document