EFFECTS OF DEXAMETHASONE, PREDNISOLONE AND CORTISOL ON THE MAST CELLS AND TISSUE EOSINOPHILS IN RAT GASTRIC MUCOSA

1962 ◽  
Vol 41 (3) ◽  
pp. 432-436 ◽  
Author(s):  
Toimi Räsänen
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Mast Cell Degranulation ◽  
The Body ◽  
Water Soluble ◽  
Soluble Form ◽  
Tissue Eosinophilia ◽  
Mucosal Mast Cells ◽  
Rat Gastric Mucosa ◽  
Intact Rats

ABSTRACT Intact rats were injected intramuscularly at 8-hourly intervals with equal amounts, 6×1.0 mg, of dexamethasone (16α-methyl-9α-fluoro-prednisolone) as phosphate, prednisolone (11β,17,21-trihydroxy-pregna-1,4-diene-3,20-dione) and cortisol (11β,17,21-trihydroxy-pregn-4-ene-3,20-dione) both as succinates, all three in water soluble form. The rats were decapitated 4 hours after the last injection and the mucosal mast cells and tissue eosinophilic cells in the body mucosa of the glandular stomach counted. Calculation of the mast cell degranulation and the destruction of tissue eosinophils during the experiment gave the following degranulation coefficients for the degranulation of gastric mucosal mast cells: 0.541 for dexamethasone, 0.177 for prednisolone and 0.088 for cortisol. The corresponding destruction coefficients for the loss of tissue eosinophilia were 0.858, 0.156 and 0.124. It is suggested that the degranulation and destruction coefficients obtained in the investigation are correlated with the catabolic biological activity of the glucocorticoids.

EFFECTS OF HEPARIN AND ASBESTOS WITH CORTICOTROPHIN ON THE MUCOSAL MAST CELLS AND TISSUE EOSINOPHILS OF RAT STOMACH

1962 ◽  
Vol 41 (3) ◽  
pp. 437-440
Author(s):  
Toimi Räsänen
Keyword(s):  
Mast Cells ◽  
Inhibitory Effect ◽  
The Body ◽  
Destructive Effect ◽  
Tissue Eosinophilia ◽  
Mucosal Mast Cells ◽  
Mucosal Cells ◽  
Mast Cell Count ◽  
Mucosal Lamina Propria ◽  
Intact Rats

ABSTRACT Intact rats were injected once with a suspension of asbestos and for 5 days with 2 IU of adrenocorticotrophin-zinc per day. 1.0 mg of heparin was injected intraperitoneally 9 times at 12-hourly intervals and the same amount of ACTH intramuscularly. The rats were decapitated 5 days after the injection of asbestos, 24 hours after the last ACTH injection and 3 hours after the last heparin injection. The mucosal mast cells and tissue eosinophils of the stomach were counted from the body mucosa and recorded per mm2 of tissue. Heparin caused no changes in either the mast cell count or tissue eosinophilia, nor did it bring about any changes in the degranulation of mucosal mast cells during the ACTH effect, or in the destruction of tissue eosinophilia. Asbestos peritonitis seemed to have a degranulating effect on mucosal mast cells and a destructive effect on tissue eosinophilia. It also appeared to increase the effect of ACTH on the mucosal cells. It is suggested that glucocorticoids stimulated by ACTH exert such an immediate effect on the function of the cells of the mucosal lamina propria that the inhibitory effect of heparin and asbestos is counteracted.

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.

Mast cell heterogeneity

1984 ◽  
Vol 62 (6) ◽  
pp. 734-737 ◽  
Author(s):  
F. Shanahan ◽  
J. A. Denburg ◽  
J. Bienenstock ◽  
A. D. Befus
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Connective Tissue ◽  
Regulatory Peptides ◽  
Cell Heterogeneity ◽  
Cell Secretion ◽  
Biochemical Basis ◽  
Mucosal Mast Cells ◽  
Mast Cell Heterogeneity

Increasing evidence for the existence of inter- and intra-species mast cell heterogeneity has expanded the potential biological role of this cell. Early studies suggesting that mast cells at mucosal sites differ morphologically and histochemically from connective tissue mast cells have been confirmed using isolated intestinal mucosal mast cells in the rat and more recently in man. These studies also established that mucosal mast cells are functionally distinct from connective tissue mast cells. Thus, mucosal and connective tissue mast cells differ in their responsiveness to a variety of mast cell secretagogues and antiallergic agents. Speculation about the therapeutic use of antiallergic drugs in disorders involving intestinal mast cells cannot, therefore, be based on extrapolation from studies of their effects on mast cells from other sites. Regulatory mechanisms for mast cell secretion may also be heterogeneous since mucosal mast cells differ from connective tissue mast cells in their response to a variety of physiologically occurring regulatory peptides. The development of techniques to purify isolated mast cell sub-populations will facilitate future analysis of the biochemical basis of the functional heterogeneity of mast cells.

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.

Cardiac mast cell-mediated activation of gelatinase and alteration of ventricular diastolic function

2002 ◽  
Vol 282 (6) ◽  
pp. H2152-H2158 ◽  
Author(s):  
Amanda L. Chancey ◽  
Gregory L. Brower ◽  
Joseph S. Janicki
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Marked Decrease ◽  
Volume Fraction ◽  
Normal Values ◽  
Mast Cell Degranulation ◽  
Ventricular Dilatation ◽  
Chemically Induced ◽  
Rat Hearts ◽  
Myocardial Collagen

Mast cells contain proteases capable of activating matrix metalloproteinases (MMPs). However, given the relatively low density of mast cells in the myocardium (i.e., 1.5–5.3 cells/mm2), it is unknown whether these enzymes are present in sufficient quantities in the normal heart to mediate MMP activation. Accordingly, this study sought to determine whether chemically induced degranulation of cardiac mast cells (with compound 48/80) would have an effect in isolated, blood-perfused, functioning rat hearts. Mast cell degranulation produced a 15% increase in histamine levels present in the coronary efflux, a significant increase in myocardial water (i.e., edema) relative to normal values (80.1 ± 3.4% vs. 77.4 ± 1.08%, P≤ 0.03), a substantial activation of MMP-2 (126% increase relative to controls, P ≤ 0.02), and a marked decrease in myocardial collagen volume fraction (0.46 ± 0.10% vs. 0.97 ± 0.33%, P ≤ 0.001). Furthermore, although an increase in ventricular stiffness was expected due to the extent of edema resulting from mast cell degranulation, modest ventricular dilatation was observed. These findings clearly demonstrate that the number of mast cells present in normal hearts is sufficient to mediate activation of MMPs and produce extracellular matrix degradation, thereby potentially causing subsequent ventricular dilatation.

Induced Long-Lived Mucosal Mast Cells In The Airways Arise From Circulating Mast Cell Progenitors

2014 ◽  
Vol 133 (2) ◽  
pp. AB145
Author(s):  
Lora Georgieva Bankova ◽  
Daniel Dwyer ◽  
Anne Y. Liu ◽  
Tatiana Jones ◽  
K. Frank Austen ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Mucosal Mast Cells

scholarly journals Adenosine A2Areceptor activation reduces infarct size in the isolated, perfused mouse heart by inhibiting resident cardiac mast cell degranulation

2008 ◽  
Vol 295 (5) ◽  
pp. H1825-H1833 ◽  
Author(s):  
Tyler H. Rork ◽  
Kori L. Wallace ◽  
Dylan P. Kennedy ◽  
Melissa A. Marshall ◽  
Amy R. Lankford ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Mast Cell ◽  
Mast Cells ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Mast Cell Degranulation ◽  
Chimeric Mice ◽  
Cgs 21680 ◽  
Perfused Hearts

Mast cells are found in the heart and contribute to reperfusion injury following myocardial ischemia. Since the activation of A2Aadenosine receptors (A2AARs) inhibits reperfusion injury, we hypothesized that ATL146e (a selective A2AAR agonist) might protect hearts in part by reducing cardiac mast cell degranulation. Hearts were isolated from five groups of congenic mice: A2AAR+/+mice, A2AAR−/−mice, mast cell-deficient (KitW-sh/W-sh) mice, and chimeric mice prepared by transplanting bone marrow from A2AAR−/−or A2AAR+/+mice to radiation-ablated A2AAR+/+mice. Six weeks after bone marrow transplantation, cardiac mast cells were repopulated with >90% donor cells. In isolated, perfused hearts subjected to ischemia-reperfusion injury, ATL146e or CGS-21680 (100 nmol/l) decreased infarct size (IS; percent area at risk) from 38 ± 2% to 24 ± 2% and 22 ± 2% in ATL146e- and CGS-21680-treated hearts, respectively ( P < 0.05) and significantly reduced mast cell degranulation, measured as tryptase release into reperfusion buffer. These changes were absent in A2AAR−/−hearts and in hearts from chimeric mice with A2AAR−/−bone marrow. Vehicle-treated KitW-sh/W-shmice had lower IS (11 ± 3%) than WT mice, and ATL146e had no significant protective effect (16 ± 3%). These data suggest that in ex vivo, buffer-perfused hearts, mast cell degranulation contributes to ischemia-reperfusion injury. In addition, our data suggest that A2AAR activation is cardioprotective in the isolated heart, at least in part by attenuating resident mast cell degranulation.

Arteriolar constriction in skeletal muscle during vascular stunning: role of mast cells

1997 ◽  
Vol 272 (5) ◽  
pp. H2154-H2163 ◽  
Author(s):  
M. W. Keller
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Vascular Reactivity ◽  
Striated Muscle ◽  
Mast Cell Degranulation ◽  
Response Curves ◽  
Maximal Diameter ◽  
Muscle Tissues ◽  
Stimulation Of

Striated muscle becomes stunned during reperfusion after sublethal ischemia. Resistance vessel tone and reactivity are altered in stunned muscle tissues. The hypothesis that adenosine-regulated mast cell degranulation occurs during reperfusion and leads to constriction of resistance arterioles was tested. The hamster cremaster muscle was subjected to 1 h of ischemia followed by reperfusion. Resistance arterioles constricted during reperfusion (74% of maximal diameter at baseline vs. 42% of maximal diameter after 30 min of reperfusion; P < 0.01). Mast cells degranulated in reperfusion concomitant with arteriolar constriction. Stimulation of mast cell degranulation in control animals with compound 48/80 or cold superfusate (21 degrees C) caused vasoconstriction that mimicked that seen in reperfusion. The mast cell stabilizer cromolyn blocked degranulation and constriction. If mast cell granules were depleted by applying compound 48/80 before inducing ischemia, then arterioles failed to constrict during reperfusion. Adenosine A3-antagonist BW-A1433 abolished constriction. These findings suggest that arterioles constrict in reperfusion due to adenosine-regulated mast cell degranulation. Vasodilation in response to sodium nitroprusside and acetylcholine was normal in stunned, constricted arterioles. However, the dose-response curves to adenosine were shifted to the left in arterioles constricted by either stunning, compound 48/80, exposure to cold superfusate, or cromolyn compared with control vessels. Depletion of granular components via stunning, compound 48/80, cold superfusate, or inhibition of secretion with cromolyn results in unopposed A1- or A2-mediated vasodilation in response to adenosine, whereas the dilatory effects of adenosine are blunted by simultaneous release of vasoconstrictors from mast cells in control animals. In summary, it was found that mast cell degranulation occurs during reperfusion and leads to constriction of resistance arterioles and altered vascular reactivity to adenosine. Adenosine is released in ischemia and stimulates mast cell degranulation via the A3 receptor located on mast cells during reperfusion.

Mucosal mast cells are involved in CCK disruption of MMC in the rat intestine

1998 ◽  
Vol 275 (1) ◽  
pp. G63-G67 ◽  
Author(s):  
Carme Juanola ◽  
Magda Giralt ◽  
Marcel Jiménez ◽  
Marisabel Mourelle ◽  
Patri Vergara
Keyword(s):  
Mast Cell ◽  
Small Intestine ◽  
Mast Cells ◽  
Control Group ◽  
Rat Intestine ◽  
Pancreatic Acini ◽  
Mast Cell Stabilizer ◽  
Mucosal Mast Cells ◽  
Stimulation Of ◽  
Cck Release

Our aim was to determine if mucosal mast cells could be activated by endogenous CCK and, as a consequence, mediate CCK actions in the small intestine. Rats were prepared for electromyography to record electrical activity in the small intestine. In another group of animals, the duodenum was perfused to measure rat mast cell protease II (RMCP II) as indicative of mast cell degranulation. Endogenous CCK release was induced by administration of soybean trypsin inhibitor (SBTI) in conscious rats or by intraduodenal perfusion of ovalbumin hydrolysate (OVH) in anesthetized rats. CCK concentration was measured by bioassay on pancreatic acini. SBTI in control rats disrupted migrating motor complexes (MMC) for >40 min. In rats treated with the mast cell stabilizer ketotifen, SBTI did not induce any change in the MMC pattern. RMCP II concentration in the duodenal perfusate significantly increased after OVH. Perfusate from ketotifen-treated animals did not show any significant increase in RMCP II values during OVH perfusion, although CCK plasma concentration was not different from the control group. Furthermore, infusion of the CCK-B receptor antagonist L-365,260 significantly blocked the increase of RMCP II concentration after OVH. Our results indicate that mucosal mast cells are degranulated by endogenous CCK release through stimulation of CCK-B receptors. Therefore mucosal mast cells participate in CCK intestinal actions.

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