scholarly journals The effect of vitamin E on mast cells in small intestine of broilers under heat stress

2018 ◽  
Vol 68 (2) ◽  
pp. 159
Author(s):  
M. YILDIZ ◽  
S. KUM ◽  
U. EREN
Keyword(s):  
Mast Cell ◽  
Small Intestine ◽  
Heat Stress ◽  
Vitamin E ◽  
Mast Cells ◽  
Broiler Chicks ◽  
Acetate Solution ◽  
Tissue Samples ◽  
Safranin O ◽  
Mast Cell Population

The aim of this study is to identify the effect of vitamin E (DL-α-tocopherol acetate) (300 IU/kg) on mast cells in the small intestine (duodenum, jejunum and ileum) under heat stress. In the study, 42 one-day-old Ross 308 male broiler chicks were used. The chicks were randomly separated into 3 groups as follows; control (22±2°C), heat stress (35°C, 5 hours/per day) and vitamin E (300 IU/kg/per day) + heat stress (35°C, 5 hours/per day). The applications of heat stress and vitamin E began on the fifteenth day and ended on the thirty-fifth day. Tissue samples were taken from animals in each group of four and five-week-old chickens. Tissue samples were fixed in BLA (Basic Lead Acetate) solution. The sections were stained with toluidine blue (TB) (pH 0.5) and alcian blue-critical electrolyte concentration (AB-CEC) (pH 5.8, 0.3 M MgCl2) / Safranin O (SO) (pH 1.0) combined method. It was determined that increasing of the exposure duration to heat stress increased the number of mast cells in the small intestine of the boilers. Also, it was revealed that vitamin E reduced mast cell population under heat stress. Consequently, heat stress may play a role in the pathogenesis of small intestine-associated with disorders and the supplementation of vitamin E can contribute to regulate small intestine functions of broilers by decreasing mast cell proliferation and activation under heat stress.

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.

scholarly journals Innervation of enteric mast cells by primary spinal afferents in guinea pig and human small intestine

2014 ◽  
Vol 307 (7) ◽  
pp. G719-G731 ◽  
Author(s):  
Guo-Du Wang ◽  
Xi-Yu Wang ◽  
Sumei Liu ◽  
Meihua Qu ◽  
Yun Xia ◽  
...  
Keyword(s):  
Nervous System ◽  
Mast Cell ◽  
Small Intestine ◽  
Electrical Stimulation ◽  
Mast Cells ◽  
Guinea Pig ◽  
Mast Cell Protease ◽  
Human Small Intestine ◽  
Neurokinin 1 ◽  
Stimulation Of

Mast cells express the substance P (SP) neurokinin 1 receptor and the calcitonin gene-related peptide (CGRP) receptor in guinea pig and human small intestine. Enzyme-linked immunoassay showed that activation of intramural afferents by antidromic electrical stimulation or by capsaicin released SP and CGRP from human and guinea pig intestinal segments. Electrical stimulation of the afferents evoked slow excitatory postsynaptic potentials (EPSPs) in the enteric nervous system. The slow EPSPs were mediated by tachykinin neurokinin 1 and CGRP receptors. Capsaicin evoked slow EPSP-like responses that were suppressed by antagonists for protease-activated receptor 2. Afferent stimulation evoked slow EPSP-like excitation that was suppressed by mast cell-stabilizing drugs. Histamine and mast cell protease II were released by 1) exposure to SP or CGRP, 2) capsaicin, 3) compound 48/80, 4) elevation of mast cell Ca2+ by ionophore A23187, and 5) antidromic electrical stimulation of afferents. The mast cell stabilizers cromolyn and doxantrazole suppressed release of protease II and histamine when evoked by SP, CGRP, capsaicin, A23187, electrical stimulation of afferents, or compound 48/80. Neural blockade by tetrodotoxin prevented mast cell protease II release in response to antidromic electrical stimulation of mesenteric afferents. The results support a hypothesis that afferent innervation of enteric mast cells releases histamine and mast cell protease II, both of which are known to act in a diffuse paracrine manner to influence the behavior of enteric nervous system neurons and to elevate the sensitivity of spinal afferent terminals.

scholarly journals Cloning of the cDNA encoding mast cell tryptase of Mongolian gerbil, Meriones unguiculatus, and its preferential expression in the intestinal mucosa

1995 ◽  
Vol 309 (3) ◽  
pp. 921-926 ◽  
Author(s):  
Y Murakumo ◽  
H Ide ◽  
H Itoh ◽  
M Tomita ◽  
T Kobayashi ◽  
...  
Keyword(s):  
Amino Acids ◽  
Mast Cell ◽  
Small Intestine ◽  
Mast Cells ◽  
Intestinal Mucosa ◽  
Mongolian Gerbil ◽  
Meriones Unguiculatus ◽  
Amino Acid Sequences ◽  
Mast Cell Tryptase ◽  
Mucosal Mast Cells

By using the combination of reverse-transcription PCR and rapid amplification of cDNA ends methods, a cDNA encoding mast cell tryptase was successfully cloned from the small intestine of Mongolian gerbil, Meriones unguiculatus, infected with Nippostrongylus brasiliensis. The cDNA was 1219 bp long including 810 bp of an open reading frame. Based on the deduced amino acid sequences of known mast cell tryptases of other species, the gerbil mast cell tryptase (gMCT) was highly similar to mouse mast cell protease (mMCP)-7, and seems to be translated as a prepro-enzyme with 25 amino acids of signal and activation peptides and 245 amino acids of mature enzyme. The gMCT mRNA was preferentially transcribed in the intestinal mucosa and to a far lesser extent in the connective tissue such as skin and tongue. Moreover, kinetic study after infection revealed that the amount of gMCT mRNA in the small intestine correlated well with the degree of intestinal mastocytosis. Throughout the course of infection, enzyme-histochemically detectable tryptase activity was limited to mucosal mast cells. Since mucosal mast cells of other rodents, including mice and rats, do not express tryptases, this is the first report of rodent mast cell tryptase expressed in the intestinal mucosa.

scholarly journals The Equine Endometrial Mast Cell during the Puerperal Period: Evaluation of Mast Cell Numbers and Types in Comparison to Other Inflammatory Changes

1997 ◽  
Vol 34 (1) ◽  
pp. 23-30 ◽  
Author(s):  
M. M. Welle ◽  
L. Audigé ◽  
J.-P. Belz
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Immunohistochemical Staining ◽  
Staining Technique ◽  
Cell Types ◽  
Postnatal Period ◽  
Double Labeling ◽  
Tissue Samples ◽  
Cell Numbers ◽  
Significant Difference

Endometrial biopsies of 44 broodmares were histologically examined on days 3, 6, and 9 postpartum. The mares were subdivided into three groups according to the course of the puerperal period. In 29 mares, parturition and expulsion of the placenta was normal, six mares showed dystocia, and in nine mares, the placenta was retained for >2 hours. Tissue samples were evaluated histologically, and the average numbers of granulocytes, lymphocytes, macrophages, siderophages, and mast cells was determined. Protease content of mast cells was examined with a double-enzyme immunohistochemical staining technique, using a histochemical reaction for chloroacetate esterase and fast blue to detect chymase activity and an immunohistochemical staining method with a polyclonal antibody and fast red for the detection of tryptase. Analyzing the cell numbers using the statistical software Statistica, a marked inflammatory reaction was observed in the endometrium postpartum. Although the number of granulocytes decreased during the first 9 days postpartum, the number of lymphocytes, macrophages, and siderophages increased. No significant difference in the number of any of these cell types could be demonstrated in the three different courses of the puerperal period, although the numbers of these cells seemed to be lower in mares with dystocia. In contrast with other cells, no change in the number of endometrial mast cells was observed during the puerperal period, but a significantly lower number were found in the endometrium of mares with retained placenta. The enzyme immunohistochemical double-labeling technique could demonstrate only tryptase-positive mast cells; no chymase activity was detectable in any endometrial mast cells. The number of mast cells detected with the metachromatic staining technique was significantly higher than that detected with double labeling. These results support the hypothesis that a sufficient number of mast cells may be necessary for a normal postnatal period and suggest a mast cell subtype in the equine endometrium that is tryptase and chymase negative.

Cerebral vasospasm: presence of mast cells in human cerebral arteries after aneurysm rupture

1981 ◽  
Vol 54 (6) ◽  
pp. 733-735 ◽  
Author(s):  
Luiz C. M. Faleiro ◽  
Conceição R. S. Machado ◽  
Amado Gripp ◽  
Rubens A. Resende ◽  
Pedro A. Rodrigues
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Cell Population ◽  
Hydrolytic Enzymes ◽  
Aneurysm Rupture ◽  
Blue Staining ◽  
Control Group ◽  
Preliminary Note ◽  
Muscular Layer ◽  
Mast Cell Population

✓ Mast cells contain heparin, histamine, hydrolytic enzymes, and possibly serotonin in metachromatic cytoplasmic granules, and are not visualized in routine histological preparations. Special fixation, frozen sections, and toluidine blue staining are essential for counting the number of mast cells in tissue sections. Histological preparations for counting mast cells were made from arteries of the circle of Willis in persons who died after chest or abdominal trauma (control group) and in patients who had subarachnoid hemorrhage (SAH) after aneurysm rupture. The arteries were removed within 6 hours of death, taking care to avoid damage to their structure, and were immersed in the fixative solution. This preliminary note, reporting findings in only a few cases, is justified by the interesting discovery of a marked increase in mast cell population in the muscular layer of arteries after SAH. The series is small because of the difficulty in obtaining suitable material, since mast cells virtually disappear when autopsy is performed later than 6 hours after death. It is concluded from this study that there is an increase of mast cell population in cerebral arterial walls after SAH, mainly in the muscular layer, and that the number of mast cells is higher in arteries closer to the aneurysm.

scholarly journals Tryptase Profile of the Rat Skin Mast Cell Population During the Wound Healing

2021 ◽  
Vol 9 (4) ◽  
pp. 84-89
Author(s):  
V. V. Shishkina ◽  
S. V. Klochkova ◽  
N. T. Alexeeva ◽  
M. Yu. Soboleva ◽  
D. I. Esaulenko ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Cell Population ◽  
Biological Activities ◽  
Repair Process ◽  
Fiber Formation ◽  
Control Group ◽  
Rat Skin ◽  
Wide Range ◽  
Mast Cell Population

Mast cells cyclically synthesize and excrete a wide range of biogenesis products with different biological activities into the extracellular matrix and are regulators of local homeostasis both in normal conditions and in pathology – inflammation, oncogenesis, etc. The relative specificity of classical histochemical methods for detecting mast cells in relation to chromogenic to substrates causes certain difficulties in the selective study of the components of the secretome of mast cells, for example, heparin, histamine, chymase or tryptase. Therefore, immunomorphological techniques have become very popular, which identify specific substrates and allow differentiation of the components of the mast cell secretome. Mediators produced by mast cells promote neoangiogenesis, fibrillogenesis and re-epithelialization during the repair process.The aim of our work was to study the tryptase profile of the mast cell population of rat skin during the wound processusing an original combined method of immunohistochemical staining.Material and methods. The experiment involved 12 Wistar rats divided into two groups – intact (n=6) and with the existing wound process of the skin in the withers (n=6). The tryptase profile of mast cells was assessed on the 7th day of the wound process in comparison with the control group.Results. The results obtained showed a significant increase in the number of tryptase-positive mast cells on the 7th day of the wound process in the skin against the background of a general increase in the population of mast cells. Intragranular tryptase reserve was significantly increased. In contrast to the control, where mast cells with single tryptase-positive granules dominated, during the wound process, cells of this type were practically not detected in the skin (43.69±2.9% and 8.55±0.9%). The content of tryptase-positive mast cells with complete filling of the cytoplasm in the control group and the group of animals with a wound process was 14.24±1.2% and 38.03±2.9%, respectively.Conclusion. Thus, when modeling a wound, an increase in tryptase synthesis is detected both in individual MCs and within the entire MC population. This fact indicates that mast cell proteases can become a potential therapeutic target for improving wound regeneration by correcting immunogenesis, inflammation and fiber formation.

Preferential Uptake of Gamma Tocopherol by Mast Cells. Does This Uptake Affect Mast Cell Cytokine Production?.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 3793-3793
Author(s):  
Omar S. Aljitawi ◽  
Mathew Fitzgerald ◽  
Min Qui ◽  
Koyamangalath Krishnan ◽  
William L. Stone ◽  
...  
Keyword(s):  
Mast Cell ◽  
Vitamin E ◽  
Mast Cells ◽  
Cytokine Production ◽  
Ppar Gamma ◽  
Alpha Tocopherol ◽  
Human Mast Cell ◽  
Peroxisome Proliferator ◽  
Gamma Tocopherol ◽  
Cell Cytokine Production

Abstract Vitamin E, the main lipid soluble antioxidant, exists in eight different forms, of which α-tocopherol and γ-tocopherol are the two major forms. Previous experiments showed vitamin E uptake by macrophages that contribute to inflammation and immunity. On the other hand, vitamin E has structural similarity to the thiazolidinedione, troglitazone, a peroxisome proliferator-activated receptor (PPAR) agonist. In previous experiments we found that troglitazone (TGZ), a PPAR gamma agonist, had a negative effect on mast cell cytokine production. We therefore wondered whether vitamin E enters human mast cells, and if so, does this modulate mast cell cytokine production? We choose (interleukin) IL-6 for its pro-inflammatory properties and because it’s known to be produced by mast cells in response to stimulants used in the experiment. In this study we try to answer these two questions. Cultured human mast cell line (HMC-1) was first incubated for 24 hrs with pharmacological concentrations of both alpha and gamma forms of vitamin E (10 μM). The mast cells were then activated with phorbol-12-myristate-13-acetate [PMA (50ng/ml)] and ionomycin (5μm) for 24 hours and cell-free supernatants collected. In additional experiments, IL-1ß (10ng/mL) was added to activate mast cells. IL-6 levels in the supernatants were determined in each well utilizing ELISA. Mast cell concentrations of alpha or gamma tocopherol were measured by high pressure liquid chromatography [HPLC] and electrochemical analysis. Mast cells pre-incubated in alpha and gamma forms of vitamin E at 10 μM did not affect mast cell IL-6 production. Mast cells, however, showed uptake of both forms of tocopherols but more pronounced uptake of the gamma form (13181.05 pmole/well of gamma compared to 8742.99 pmole/well of alpha tocopherol). We conclude that mast cells appear to store both alpha and gamma tocopherols but preferentially more gamma tocopherol. Though Vitamin E and PPAR agonists have similar structures, they did not show similar effect on mast cell cytokine production, suggesting they might have different mechanisms of action.

scholarly journals Effects of heat stress on somatostatin and some related immune factors in the small intestine of Wenchang chicks

2017 ◽  
Vol 62 (No. 10) ◽  
pp. 446-455 ◽  
Author(s):  
Z. Chen ◽  
Y.-Y. Jiang ◽  
Y.-W. Zhou ◽  
C. Liang ◽  
L.-J. Xie
Keyword(s):  
Small Intestine ◽  
Heat Stress ◽  
Intestinal Mucosa ◽  
Statistical Significance ◽  
Broiler Chicks ◽  
Immune Functions ◽  
Intestinal Segments ◽  
Protection Mechanisms ◽  
Immune Factors ◽  
Self Protection

To investigate the effects of heat stress (HS) on developmental changes in immune functions of chick intestinal mucosa, one-day-old broiler chicks were randomly assigned into control check (CK) and heat-stressed (HS) groups and raised under indoor temperature. The chicks in HS group were subjected to HS at 40 ± 0.5°C from 12:00 to14:00 h every day. Intestinal mucosa samples were collected weekly during 6 weeks, and the effects of HS on somatostatin and its related immune factors were examined using immunohistochemical, physiological, and biochemical methods. The results showed that HS obviously increased the amount and integral optical density of somatostatin positive cells, somatostatin content, as well as IFN-γ and IL-2 levels in the small intestine, and these increases reached statistical significance in some intestinal segments (P < 0.05). In addition, IgG, IgA, and IgM levels fluctuated in different intestinal segments and their levels in jejunum, duodenum, and ileum in 6-week-old chicks were significantly lower in HS group than in CK group (P < 0.05). The contents of immune-related enzymes also fluctuated, but the activities of acid phosphatase, lysozyme, and glutathione reductase in duodenum and jejunum were lower in 6-week-old chicks in HS group than in CK group, some reaching statistical significance (P < 0.05). Growth hormone (GH) and HSP70 contents in multiple intestinal segments in 6-week-old chicks were significantly higher in HS group than in CK group (P < 0.05). The results indicate that (1) HS could increase the expression and secretion of somatostatin and affect the normal development of immunoglobulins, cytokines, and immune-related enzymes in the small intestine, and thereby impact the chicks’ intestine immune function; (2) GH and HSP70 in the small intestine were involved in self-protection mechanisms against HS-induced intestinal injury and somatostatin regulation might be one of the important components.

Histamine sensitivity of mesenteric afferent nerves in the rat jejunum

1998 ◽  
Vol 275 (4) ◽  
pp. G675-G680 ◽  
Author(s):  
M. E. Kreis ◽  
W. Haupt ◽  
A. J. Kirkup ◽  
D. Grundy
Keyword(s):  
Mast Cell ◽  
Small Intestine ◽  
Mast Cells ◽  
Receptor Agonist ◽  
Rat Jejunum ◽  
Functional Interaction ◽  
Afferent Nerves ◽  
Afferent Discharge ◽  
Dose Dependent ◽  
Nerve Communication

The concept of functional interaction between mast cells and intestinal afferents is gaining support. We have therefore characterized the action of histamine on jejunal afferent discharge in the anesthetized rat. Whole nerve mesenteric afferent discharge was recorded in conjunction with intestinal pressure in response to a range of histamine agonists and antagonists. Histamine at 2, 4, and 8 μmol/kg (iv) evoked a dose-dependent biphasic increase in afferent discharge together with a biphasic rise in intestinal pressure. However, these two events were mediated independently, since nifedipine (1 mg/kg) substantially reduced the intestinal pressure increase but not the afferent discharge. These responses were completely inhibited by pyrilamine (5 mg/kg) but unaffected by ranitidine (5 mg/kg) or thioperamide (2 mg/kg). Neither the selective H2receptor agonist dimaprit nor the selective H3receptor agonist R-α-methylhistamine caused any modulation of afferent discharge. We conclude that histamine stimulates an H1receptor-mediated increase in mesenteric afferent discharge that is independent of intestinal motor events. This suggests that histamine potentially acts as a mediator in mast cell-to-afferent nerve communication in the small intestine.

scholarly journals Notch2 signaling is required for proper mast cell distribution and mucosal immunity in the intestine

Blood ◽  
2011 ◽  
Vol 117 (1) ◽  
pp. 128-134 ◽  
Author(s):  
Mamiko Sakata-Yanagimoto ◽  
Toru Sakai ◽  
Yasuyuki Miyake ◽  
Toshiki I. Saito ◽  
Haruhiko Maruyama ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Mast Cell ◽  
Small Intestine ◽  
Mast Cells ◽  
Lamina Propria ◽  
Conditional Knockout ◽  
Small Intestinal Mucosa ◽  
Epithelial Layer ◽  
Strongyloides Venezuelensis ◽  
Small Intestinal

Abstract Notch receptor-mediated signaling is involved in the developmental process and functional modulation of lymphocytes, as well as in mast cell differentiation. Here, we investigated whether Notch signaling is required for antipathogen host defense regulated by mast cells. Mast cells were rarely found in the small intestine of wild-type C57BL/6 mice but accumulated abnormally in the lamina propria of the small-intestinal mucosa of the Notch2-conditional knockout mice in naive status. When transplanted into mast cell–deficient Wsh/Wsh mice, Notch2-null bone marrow-derived mast cells were rarely found within the epithelial layer but abnormally localized to the lamina propria, whereas control bone marrow-derived mast cells were mainly found within the epithelial layer. After the infection of Notch2 knockout and control mice with L3 larvae of Strongyloides venezuelensis, the abundant number of mast cells was rapidly mobilized to the epithelial layer in the control mice. In contrast, mast cells were massively accumulated in the lamina propria of the small intestinal mucosa in Notch2-conditional knockout mice, accompanied by impaired eradication of Strongyloides venezuelensis. These findings indicate that cell-autonomous Notch2 signaling in mast cells is required for proper localization of intestinal mast cells and further imply a critical role of Notch signaling in the host-pathogen interface in the small intestine.

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