scholarly journals Mast Cells and Histamine: Do They Influence Placental Vascular Network and Development in Preeclampsia?

2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
Grzegorz Szewczyk ◽  
Michał Pyzlak ◽  
Jakub Klimkiewicz ◽  
Wacław Śmiertka ◽  
Magdalena Miedzińska-Maciejewska ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Vascular Network ◽  
Control Group ◽  
Network Development ◽  
Mast Cell Tryptase ◽  
Differential Distribution ◽  
Histamine Concentration ◽  
Common Features ◽  
Mast Cell Density

The physiological course of pregnancy is closely related to adequate development of the placenta. Shallow invasion of trophoblast as well as decreased development of the placental vascular network are both common features of preeclampsia. To better understand the proangiogenic features of mast cells, in this study we aim to identify the potential relationship between the distribution of mast cells within the placenta and vascular network development.Material and Methods. Placentas from preeclampsia-complicated pregnancies () and from physiological pregnancies () were acquired after cesarean section. The concentration of histamine was measured, and immunohistochemical staining for mast cell tryptase was performed. Morphometric analysis was then performed.Results. We noticed significant differences between the examined groups. Notably, in the preeclampsia group compared to the control group, we observed a higher mean histamine concentration, higher mast cell density (MCD), lower mean mast cell (MMCA) and lower vascular/extravascular (V/EVT) index. In physiological pregnancies, a positive correlation was observed between the histamine concentration and V/VEVT index as well as MCD and the V/VEVT index. In contrast, a negative correlation was observed between MMCA and the V/EVT index in physiological pregnancies.Conclusions. Based on the data from our study, we suggest that a differential distribution of mast cells and corresponding changes in the concentration of histamine are involved in the defective placental vascularization seen in preeclamptic placentas.

scholarly journals Immunohistochemical analysis of the arterial supply and mast cells of the trigeminal ganglion

2021 ◽  
pp. 16-16
Author(s):  
Aleksandar Mircic ◽  
Aleksandar Malikovic ◽  
Bojan Stimec ◽  
Aleksandra Milosavljevic ◽  
Dejan Cetkovic ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Trigeminal Ganglion ◽  
Regional Differences ◽  
Immunohistochemical Analysis ◽  
Mast Cell Tryptase ◽  
Significant Statistical Difference ◽  
Migraine Pain ◽  
Mast Cell Density ◽  
Ganglionic Cell

The aim of this study was to quantify the distribution of microvessels and mast cells in all three parts of the trigeminal ganglion (TG). Statistical analyses were applied to investigate possible micromorphological regional differences in their density. Five serially sectioned human TGs were prepared for CD34 and mast cell tryptase immunostaining. The following quantifications were performed in microscopic fields of three parts of the TG: microvessel density (MVD), mast cell density (MCD) and ganglionic cell count. The density of CD34-positive microvessels was not significantly different in any of the three observed parts of the TG. The distribution of neurons showed no significant statistical difference in three parts of the TG. There was no difference in the density of tryptase-positive mast cells within the TG, but there was an abundant presence of mast cells in the periganglionic dural and subdural tissues, a finding hitherto not reported. We can say that there is a homogenous vascular pattern within the TG which excludes local predominance in pathogenesis of trigeminal neuralgia. Second, and more important, the finding of peri-trigeminal mast cells indicates their important role in migraine pain and confirms their degranulation as the main therapeutic goal for this condition.

scholarly journals Overexpression of HIF-1α and Morphological Alterations in the Tongue of Rats Exposed To Secondhand Smoke

2020 ◽  
Vol 31 (3) ◽  
pp. 281-289
Author(s):  
Eleonora de Paula Amaral ◽  
Rodrigo César Rosa ◽  
Renata Margarida Etchebehere ◽  
Ruchele Dias Nogueira ◽  
José Batista Volpon ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Cell Density ◽  
Tobacco Smoke ◽  
Secondhand Smoke ◽  
Smoke Inhalation ◽  
Lower Percentage ◽  
Control Group ◽  
Albino Rats ◽  
Mast Cell Density

Abstract Smoking is a risk factor for serious health problems and is associated with several changes in the tissues of the oral cavity. The aim of this study was to evaluate the collagen percentage, mast cells density, intensity of immunolabeled cells by anti-HIF-1α in the musculature lingual of rats exposed to secondhand smoke. Twenty-seven female Wistar albino rats were divided into three groups: rats not exposed to tobacco smoke inhalation (Control group) (n=7); rats exposed to smoke inhalation for 30 days (TAB 30) (n=10); and rats exposed to smoke inhalation for 45 days (TAB 45) (n=10). Subsequently, the animals were submitted to euthanasia and removal of the tongue for histological and immunohistochemistry processing and analysis. In the groups TAB 30 and TAB 45 there were a lower percentage of collagen, a higher density of mast cells and a greater intensity of anti-HIF-1α immunolabeled cells compared to Control group. There was also a positive and significant correlation between the percentage of collagen and mast cell density. There was not significative difference between TAB 30 e TAB 45 in any of the parameters evaluated. Therefore, the exposure of rats to secondhand smoke for 45 days causes decrease in perimysial collagen fibers, increase in the number of mast cells and increase in the immunolabeling for HIF-1α in lingual muscle cells. The present study was the first to evaluate the percentage of collagen, mast cell density and immunostaining for HIF-1α in rat tongues exposed to tobacco smoke.

Lung mast cell density and distribution in chronically hypoxic animals

1977 ◽  
Vol 42 (2) ◽  
pp. 174-178 ◽  
Author(s):  
A. Tucker ◽  
I. F. McMurtry ◽  
A. F. Alexander ◽  
J. T. Reeves ◽  
R. F. Grover
Keyword(s):  
Cell Proliferation ◽  
Pulmonary Hypertension ◽  
Mast Cell ◽  
Mast Cells ◽  
Cell Density ◽  
Mammalian Species ◽  
Cell Hyperplasia ◽  
Mast Cell Density ◽  
Lung Mast Cell ◽  
Mast Cell Hyperplasia

Changes in the density and distribution of pulmonary mast cells were determined in six mammalian species exposed to hypobaric hypoxia (PB = 435 Torr) for 19–48 days. Control animals were studied at 1,600 m (PB = 635 Torr). Total lung mast cell hyperplasia was observed only in calves exposed to high altitude. Pigs, rats, and sheep exhibited small, but insignificant, increases in mast cell density. Perivascular mast cell proliferation adjacent to vessels of 30–500 mum in diameter was seen in both calves and pigs. Bronchial, alveolar septal, and systemic tissue (tongue) mast cell hyperplasia was not observed in any of the species. Three indices of pulmonary hypertension (right ventricular hypertrophy, medial thickness of pulmonary arteries, and pulmonary arterial pressure) correlated with perivascular mast cell density. The findings indicate that perivascular mast cell proliferation may relate more to the morphological pulmonary vascular changes and to pulmonary hypertension than to hypoxia, leading to the speculation that mast cells increase in number in response to the hypertension, rather than to mediate and maintain the hypertension.

Mastocytic Enterocolitis: Increased Mucosal Mast Cells in Chronic Intractable Diarrhea

2006 ◽  
Vol 130 (3) ◽  
pp. 362-367 ◽  
Author(s):  
Shriram Jakate ◽  
Mark Demeo ◽  
Rohan John ◽  
Mary Tobin ◽  
Ali Keshavarzian
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
High Power ◽  
Chronic Diarrhea ◽  
Duodenal Biopsy ◽  
Mast Cell Tryptase ◽  
High Power Field ◽  
Intractable Diarrhea ◽  
Biopsy Specimens ◽  
Hematoxylin Eosin

Abstract Context.—In some adult patients with chronic intractable diarrhea, the diagnosis remains elusive even after detailed evaluations, and colonic or duodenal biopsy specimens may appear unremarkable on routine hematoxylin-eosin staining. Objectives.—To assess the concentration of mast cells in colonic or duodenal biopsy specimens by immunohistochemical analysis for mast cell tryptase from patients with chronic intractable diarrhea and to evaluate their response to drugs affecting mast cell function. Design.—Mast cells per high-power field were assessed in biopsy specimens from 47 patients with chronic intractable diarrhea, from 50 control subjects, and from 63 patients with other specific diseases that cause chronic diarrhea (inflammatory bowel disease, celiac disease, collagenous colitis, and lymphocytic colitis). Patients with chronic intractable diarrhea who had more than 20 mast cells per high-power field were administered drugs affecting mast cell mediator function and release. Results.—The mean ± SD concentration of mast cells in the 50 control subjects was 13.3 ± 3.5 cells per high-power field; hence, patients with more than 20 mast cells per high-power field were considered to have increased mast cells. Thirty-three (70%) of 47 patients with chronic intractable diarrhea had increased mast cells, and symptoms were controlled by drug therapy in 22 (67%) of the 33 patients. No patient had systemic or cutaneous mastocytosis. No increase in mast cells was seen in patients with other common causes of chronic diarrhea. Conclusions.—In chronic intractable diarrhea, colonic or duodenal biopsy specimens may appear unremarkable on routine hematoxylin-eosin staining, but increased mast cells may be demonstrated by immunohistochemistry for mast cell tryptase, with the novel term mastocytic enterocolitis describing this condition. Similar increases in mast cells are not apparent in control populations or in patients with other specific diseases that cause chronic diarrhea. The cause of the increased mast cells remains to be elucidated.

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.

Inhibitory Effect of Retinoic Acid on Proliferation, Maturation and Tryptase Level in Human Leukemic Mast Cells (HMC-1)

2003 ◽  
Vol 16 (1) ◽  
pp. 43-47 ◽  
Author(s):  
M.G. Alexandrakis ◽  
D.S. Kyriakou ◽  
D. Seretakis ◽  
W. Boucher ◽  
R. Letourneau ◽  
...  
Keyword(s):  
Mast Cell ◽  
Retinoic Acid ◽  
Mast Cells ◽  
Allergic Inflammation ◽  
Inhibitory Effect ◽  
Control Group ◽  
Tryptase Level ◽  
Synthetic Derivatives ◽  
Derivatives Of ◽  
Inhibit Cell Proliferation

Mast cells play an important role in allergic inflammation by releasing histamine, tryptase and several inflammatory cytokines. Human leukemic mast cells (HMC-1) have been used to study mast cell mediators and their role in inflammatory mechanisms. HMC-1 contain and release several inflammatory mediators, of which the proteolytic enzyme tryptase is most characteristic. Retinoids, including retinoic acid, are naturally occurring and synthetic derivatives of vitamin A. All-trans-retinoic (ATRA) acid had been previously reported to inhibit cell proliferation, differentiation and apoptosis. In the present study, we investigated the effect of ATRA on the proliferation and secretion of tryptase in HMC-1. HMC-1 were treated with ATRA at 10-4M, 10-5M or 10-6M for 3,4 or 5 days in culture. Control HMC-1 were treated with equal amount of culture medium only. ATRA decreased the number of HMC-1 as compared to the control group. The same treatment for 3, 4 or 5 days also decreased intracellular tryptase levels. These results indicate that ATRA significantly inhibits both proliferation and growth as shown by the decreased intracellular tryptase levels in HMC-1. ATRA may be a useful agent in the treatment of mast cell proliferative disorders.

Effects of nonselective endothelin-1 receptor antagonism on cardiac mast cell-mediated ventricular remodeling in rats

2008 ◽  
Vol 294 (3) ◽  
pp. H1251-H1257 ◽  
Author(s):  
David B. Murray ◽  
Jason D. Gardner ◽  
Gregory L. Brower ◽  
Joseph S. Janicki
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Cell Density ◽  
Volume Fraction ◽  
Volume Overload ◽  
Receptor Antagonism ◽  
Collagen Volume Fraction ◽  
Endothelin 1 ◽  
Mast Cell Density ◽  
Chronic Volume Overload

The objective of this study was to investigate the effect a nonselective endothelin-1 (ET-1) receptor antagonist (bosentan) had on the acute myocardial remodeling process including left ventricular (LV) mast cells and matrix metalloproteinase (MMP) activity secondary to volume overload. Additionally, we investigated the overall functional outcome of preventative endothelin receptor antagonism during 14 days of chronic volume overload. LV tissue from sham-operated (Sham), untreated-fistula (Fist), and bosentan (100 mg·kg−1·day−1)-treated animals (Fist + Bos) was analyzed for mast cell density, MMP activity, and myocardial collagen volume fraction at 1 and 5 days after the creation of an aortocaval fistula. When compared with untreated fistulas, bosentan treatment prevented the marked increase in LV mast cell density at 1 day postfistula (3.1 ± 0.3 vs. 1.3 ± 0.3 LV mast cells/mm2, Fist vs. Fist + Bos, P ≤ 0.01). Additionally, the substantial increase in MMP-2 activation in the untreated fistula at 1 day was prevented following bosentan treatment (1.6 ± 0.3 vs. 0.9 ± 0.1 arbitrary activity units, Fist vs. Fist + Bos, P ≤ 0.01). The marked decrease in collagen volume fraction seen in the Fist group (1.4 ± 0.1 vs. 0.8 ± 0.1% myocardial tissue, Sham vs. Fist, P ≤ 0.01) was significantly attenuated following bosentan treatment at both the 1- and 5-day time points. Lastly, a 2-wk preventative treatment with bosentan resulted in significant attenuation of the increase in LV end-systolic and -diastolic volumes compared with those in untreated fistula hearts. In summary, nonselective ET-1 antagonism prevents the acute increases in cardiac mast cell density and MMP activation induced secondary to chronic volume overload. By preventing these events, ET-1 antagonism was efficacious in attenuating ventricular dilatation and limiting the development of structural and functional deficits in the first 2 wk of chronic volume overload. Accordingly, these results are the first to demonstrate that cardiac mast cells are responsive to the endogenous endothelin system in vivo. Another novel finding from this study is that chronic nonspecific endothelin antagonism may inadvertently potentiate ET-1-mediated signaling.

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.

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 CHANGES IN SECRETION OF RAT SKIN MAST CELLS IN SYSTEMIC INFLAMMATORY RESPONSE

2020 ◽  
Vol 10 (2) ◽  
pp. 61-68
Author(s):  
N. V. Yaglova ◽  
S. S. Obernikhin ◽  
V. V. Yaglov
Keyword(s):  
Immune Response ◽  
Mast Cell ◽  
Mast Cells ◽  
Inflammatory Response ◽  
Systemic Inflammatory Response ◽  
Sublethal Dose ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Rat Skin ◽  
Functional Changes

Mast cells are active participants of innate immune response. Systemic immune response induces functional changes even in organs, which are not considered primary targets of bacterial or viral infections. Cytophysiology of mast cells located in organs not affected by systemic inflammatory response, like skin, is still poorly studied. Investiga- tions of this issue might elucidate some pathogenetic mechanism of skin diseases associated with previously devel- oped intestinal or respiratory infection. The aim was to investigate structural changes of rat skin mast cells in systemic inflammatory response indicative of mast cell secretion. Materials and methods: The experiment was performed on 45 male Wistar rats. Systemic inflammatory response was induced by intraperitoneal injection of sublethal dose of lipopolysaccharide E. coli (20mg/kg). The survived rats were sacrificed 1 and 7 days after injection. Serum levels of interleucine-2, 12p40, and interferon-γ were evaluated by enzyme-linked immunosorbent assay. Histological examination of abdominal skin slices, stained with hematoxilin and eosin and toluidine blue was performed. Results. The rats developed systemic inflammatory response, which attenuated on the 7th day after lipopolysac- charide injection. No significant changes in skin morphology were found. Skin mast cells demonstrated some morpho- logical and functional changes indicative of active secretion of mediators without activation of degranulation. On the 7th day mast cell cytophysiology had no significant changes compared to the control group. Conclusion. Systemic inflammatory response induced by bacterial lipopolysaccharide does not activate migration of mast cells to skin, but changes their secretory processes by enhancing peace-meal degranulation.

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