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.

scholarly journals Role of mucosal mast cells in early vascular permeability changes of intestinal DTH reaction in the rat

1998 ◽  
Vol 274 (5) ◽  
pp. G832-G839 ◽  
Author(s):  
Aletta D. Kraneveld ◽  
Thea Muis ◽  
Andries S. Koster ◽  
Frans P. Nijkamp
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Cell Activation ◽  
Vascular Leakage ◽  
Mast Cell Activation ◽  
Mucosal Mast Cell ◽  
Mucosal Mast Cells

Previously, it was shown that depletion and stabilization of the mucosal mast cell around the time of challenge were very effective in reducing delayed-type hypersensitivity (DTH) reactions in the small intestine of the rat. The role of mucosal mast cells in the early component of intestinal DTH reaction was further investigated in this study. In vivo small intestinal vascular leakage and serum levels of rat mast cell protease II (RMCP II) were determined within 1 h after intragastric challenge of rats that had been sensitized with dinitrobenzene 5 days before. A separate group of rats was used to study vasopermeability in isolated vascularly perfused small intestine after in vitro challenge. To investigate the effects of mast cell stabilization on the early events of the DTH reaction, doxantrazole was used. The influence of sensory nerves was studied by means of neonatal capsaicin-induced depletion of sensory neuropeptides. Within 1 h after challenge, a significant increase in vascular permeability was found in vivo as well as in vitro. This was associated with a DTH-specific increase in RMCP II in the serum, indicating mucosal mast cell activation. In addition, doxantrazole treatment and caspaicin pretreatment resulted in a significant inhibition of the DTH-induced vascular leakage and an increase in serum RMCP II. These findings are consistent with an important role for mucosal mast cells in early vascular leakage changes of intestinal DTH reactions. In addition, sensory nervous control of mucosal mast cell activation early after challenge is demonstrated.

A laboratory demonstration for learning about mast cell degranulation.

1999 ◽  
Vol 276 (6) ◽  
pp. S19
Author(s):  
J Corado ◽  
A Eblen-Zajjur
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Experimental Model ◽  
Low Cost ◽  
Mast Cell Degranulation ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

A simple experimental model of cell degranulation was implemented that exposed mast cells obtained from Sprague-Dawley rats to saponin. The model is flexible, asy, and low cost, is not very time-consuming to run, and needs a minimum of laboratory resources. It has been used for the last three years in our undergraduate medical physiology courses and has replaced the classic utilization of slides and drawings.

Ultrastructural effects of intravascularly injected polyethylene glycol-hemoglobin in intestinal mucosa

1998 ◽  
Vol 275 (2) ◽  
pp. H615-H625 ◽  
Author(s):  
Ann L. Baldwin ◽  
Lisa M. Wilson ◽  
J. Edward Valeski
Keyword(s):  
Mast Cell ◽  
Polyethylene Glycol ◽  
Intestinal Mucosa ◽  
Time Course ◽  
Mast Cell Degranulation ◽  
Intestinal Lumen ◽  
Saline Control ◽  
Mucosal Mast Cell ◽  
Sprague Dawley ◽  
Cell Secretion

Polyethylene glycol (PEG)-conjugated Hb (PEG-Hb) is being considered as a blood substitute. Previously, we showed that PEG-Hb extravasates rapidly from the intestinal mucosa and causes transient epithelial sloughing, resulting in temporary unimpeded passage of material between the intestinal lumen and the microcirculation. The present study quantifies the time course of factors related to this disturbance. Anesthetized Sprague-Dawley rats (350–450 g) were injected with a bolus of PEG-Hb (10 mg/ml) in saline. Control animals received saline, alone or with Dextran 70 (5 mg/ml). After 2, 8, 15, 60, or 90 min, the small intestine was perfusion fixed for microscopy (4 animals for each time point). Epithelial cell detachment and mucosal mast cell degranulation peaked at 2 and 8–15 min, respectively, but by 90 min were back to normal. Goblet cell secretion increased with time up to 8–15 min, after which it leveled off. Mean interstitial width was significantly greater 8 min after injection than for controls and continued to increase with time. In capillaries, endothelial fenestral diaphragms were replaced by thick, amorphous structures. Mesenteric mast cell degranulation was significantly greater 60–90 min after injection compared with controls. We propose that these results are consistent with intravascular injection of PEG-Hb invoking a transient inflammatory response in the intestine.

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.

In vitro activation of murine DRG neurons by CGRP-mediated mucosal mast cell degranulation

2004 ◽  
Vol 287 (1) ◽  
pp. G178-G191 ◽  
Author(s):  
F. De Jonge ◽  
A. De Laet ◽  
L. Van Nassauw ◽  
J. K. Brown ◽  
H. R. P. Miller ◽  
...  
Keyword(s):  
Mast Cell ◽  
Nerve Fibers ◽  
Mast Cell Degranulation ◽  
Mucosal Mast Cell ◽  
Close Apposition ◽  
Drg Neurons ◽  
Nodose Ganglia ◽  
Mouse Mast Cell

Upregulation of CGRP-immunoreactive (IR) primary afferent nerve fibers accompanied by mastocytosis is characteristic for the Schistosoma mansoni-infected murine ileum. These mucosal mast cells (MMC) and CGRP-IR fibers, which originate from dorsal root (DRG) and nodose ganglia, are found in close apposition. We examined interactions between primary cultured MMC and CGRP-IR DRG neurons in vitro by confocal recording of intracellular Ca2+concentration ([Ca2+]i). The degranulatory EC50for the mast cell secretagogue compound 48/80 (C48/80; 10 μg/ml) and the neuropeptides CGRP (2.10−8M) and substance P (SP; 3.10−8M) were determined by measurement of extracellular release of the granule chymase, mouse mast cell protease-1. Application of C48/80 (10 μg/ml) and CGRP and SP (both 10−7M) to Fluo-4-loaded MMC induced a transient rise in [Ca2+]iafter a lag time, indicative of mast cell degranulation and/or secretion. The CGRP response could be completely blocked by pertussis toxin (2 μg/ml), indicating involvement of Giproteins. Application of MMC juice, obtained by C48/80 degranulation of MMC, to Fluo-4-loaded DRG neurons induced in all neurons a rise in [Ca2+]i, indicative of activation. Degranulation of MMC by C48/80 in culture dishes containing Fluo-4-loaded DRG neurons also caused activation of the DRG neurons. In conclusion, these results demonstrate a bidirectional cross-talk between cultured MMC and CGRP-IR DRG neurons in vitro. This indicates that such a communication may be the functional relevance for the close apposition between MMC and CGRP-IR nerve fibers in vivo.

Endothelin-1 induces mucosal mast cell degranulation and tissue injury via ETA receptors

2002 ◽  
Vol 103 (s2002) ◽  
pp. 31S-34S ◽  
Author(s):  
Mihály BOROS ◽  
László SZALAY ◽  
József KASZAKI
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Receptor Antagonist ◽  
Mast Cell Degranulation ◽  
Tissue Response ◽  
Mucosal Mast Cell ◽  
Receptor Antagonists ◽  
Endothelin 1 ◽  
Eta Receptor ◽  
Etb Receptor

The effects of endothelin-1 (ET-1) on mucosal mast cells are of special interest, since they may be an important component of the tissue response that occurs during ischaemic preconditioning or ischaemia/re-oxygenation injuries. Increasing doses of ET-1 were administered intravenously to anaesthetized rats. In a second series of experiments, animals were pretreated with the ETA receptor antagonists BQ-610 or ETR-P1/fl peptide, or with the ETB receptor antagonist IRL-1038. Intestinal perfusion changes were recorded, and the proportion of degranulated mast cells and the degree of mucosal damage were determined in ileal biopsies. ET-1 induced dose-dependent alterations in the haemodynamic and morphological parameters, and caused significant mast cell degranulation. These changes were inhibited significantly by pretreatment with the ETA receptor antagonists, but not with the ETB receptor antagonist. We conclude that a cross-talk exists between endothelial cell-derived humoral mediators and the intestinal mast cell system.

scholarly journals Mucosal Mast Cells in Irritable Bowel Syndrome and Inflammatory Bowel Disease

2005 ◽  
Vol 48 (3-4) ◽  
pp. 163-164 ◽  
Author(s):  
Bilge Tunc ◽  
Levent Filik ◽  
Engin Altıntas ◽  
Nesrin Turhan ◽  
Aysel Ulker ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Mast Cell ◽  
Irritable Bowel Syndrome ◽  
Mast Cells ◽  
Bowel Disease ◽  
Mucosal Mast Cell ◽  
Cell Counts ◽  
Mucosal Mast Cells ◽  
Inflammatory Bowel ◽  
Irritable Bowel

Even though exciting progresses have been until now, further studies are necessary to clearly understand the significance of MMC. Mast cells are thought to participate in the pathogenesis of inflammatory bowel disease and irritable bowel syndrome. However, their role in the pathogenesis remains unsettled. The specific aims of this study were to (1) examine mucosal mast cell counts in the cecum in patient with IBS, and IBD (2) compare MMC between the disease groups. We showed increased MMC count in IBS.

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