Human testicular mast cells contain tryptase: increased mast cell number and altered distribution in the testes of infertile men

2000 ◽  
Vol 74 (2) ◽  
pp. 239-244 ◽  
Author(s):  
Viktor Meineke ◽  
Monica B Frungieri ◽  
Berthold Jessberger ◽  
Hermann-Josef Vogt ◽  
Artur Mayerhofer
2008 ◽  
Vol 295 (4) ◽  
pp. F1103-F1109 ◽  
Author(s):  
Pia Welker ◽  
Stephanie Krämer ◽  
David A. Groneberg ◽  
Hans H. Neumayer ◽  
Sebastian Bachmann ◽  
...  

Mast cells have recently been related to nonallergic chronic organ damage and fibrosis. In the present study, we analyzed mast cell number, localization, and maturation in the kidney of a relatively unique group of middle-aged accident victims with primary essential hypertension and in normotensive controls ( n = 8 per group, Caucasians, predominantly male). Hypertensive kidneys showed a significantly higher degree of arteriolosclerosis. However, glomerular and tubulointerstitial matrix accumulation did not differ significantly to normotensive controls indicating a relatively early stage of hypertensive nephropathy. Using toluidine blue staining, renal mast cell number was found to be fivefold higher in hypertensive subjects compared with normotensive controls. Mast cells were primarily located in the peritubular interstitial spaces, some perivascular, but not in glomeruli. In a series of immunohistological staining studies, mast cell maturation grading showed that expression of early hematopoietic precursor cell marker CD34 did not differ between both groups. In contrast, mast cells were mostly positive for IgE receptor, tryptase, and chymase indicating a mature, differentiated cell phenotype in hypertensive nephropathy. Renal expression of stem cell factor was markedly upregulated in primary hypertension. Kidney macrophage and lymphocyte numbers were similar in both groups. In conclusion, human hypertensive kidney disease shows an early and conspicuous upregulation of stem cell factor along with an increased number of mature mast cells. The results suggest that renal mast cell accumulation may play a role in the pathogenesis of human hypertensive nephropathy.


1963 ◽  
Vol 44 (4) ◽  
pp. 606-612 ◽  
Author(s):  
Robert Brunish ◽  
Bente Sørensen

ABSTRACT Carassius auratus were injected with pituitary exophthalmos-producing substance and the subsequent histological changes studied. Oedema, infiltration of macrophages in the retrobulbar area, muscle swelling and splitting, and increase of mucinous substance were noted. Since such changes have been reported for exophthalmic human patients and guinea pigs, it is suggested that the proptosis induced in fish has a genesis similar to that of the other species. Mast cells were hardly observed in Carassius auratus whenever the histological sections were exposed to aqueous solutions. With due precautions, however, an increase in mast cell number in the intestinal submucosa was noted.


2002 ◽  
Vol 283 (2) ◽  
pp. H518-H525 ◽  
Author(s):  
Gregory L. Brower ◽  
Amanda L. Chancey ◽  
Srihari Thanigaraj ◽  
Beatriz B. Matsubara ◽  
Joseph S. Janicki

The objectives of this study were to investigate the temporal response of left ventricular (LV) matrix metalloproteinase (MMP) activity and collagen volume fraction (CVF) induced by an aortocaval fistula and the role of cardiac mast cells in regulating MMP activity. LV tissue was analyzed for MMP activity, CVF, and mast cell number in rats euthanized at 0.5, 1, 2, 3, 5, 14, 21, 35, and 56 days. Additional rats treated with the mast cell membrane-stabilizing drug cromolyn sodium were euthanized 1, 2, and 3 days postfistula. Marked increases in MMP activity occurred rapidly and remained significantly elevated for 5 days before returning toward normal. A significant decrease in CVF occurred by day 5, but thereafter CVF rebounded to normal or above normal values. The number of myocardial mast cells also significantly increased postfistula, and there was a close association between mast cell density and MMP activity. Cromolyn treatment prevented the increase in mast cell number and MMP activity. Thus it is concluded that cardiac mast cells play a major role in the regulation of MMP activity.


2014 ◽  
Vol 15 (3) ◽  
pp. 300-305 ◽  
Author(s):  
Kavita Rao ◽  
NS Priya ◽  
K Uma ◽  
HS Umadevi ◽  
T Smitha

ABSTRACT Aim The aim of the study was to quantify the presence of mast cells in various inflammatory lesions like periapical granuloma, periapical cyst, inflammatory gingival hyperplasia and pyogenic granuloma. Mast cell degranulation and association with lymphocytes were also recorded in an attempt to understand the role of mast cells in the pathogenesis of these inflammatory lesions. Materials and methods The quantification of mast cells was done on toluidine blue stained sections of all the four groups of lesions, using the image analyzer software, Image-Pro-Express (Media Cybernetics, USA). Results An increased number of mast cells in various inflammatory lesions with a significant difference between the four groups were noted. Mast cell number tended to be greater in the lesions present in the anterior region of the mouth than in the posterior region of the oral cavity. The mean mast cell number decreased with the increasing age which was directly correlated with the age of the patients. Mast cell site, distribution, degranulation and its association with fibroblasts, lymphocytes and blood vessels were noted. Conclusion The location of mast cells in different areas, their association with lymphocytes, fibroblasts, endothelial cells, and the phenomenon of degranulation helps to appreciate the release of various mediators and multiple interactions among these cells, leading to increased vascular permeability, angiogenic response, collagen synthesis, regulation of inflammation, bone resorption, and extracellular matrix destruction, thus contributing to the pathogenesis of these inflammatory lesions. How to cite this article Sheethal HS, Uma K, Rao K, Priya NS, Umadevi HS, Smitha T. A Quantitative Analysis of Mast Cells in Inflammatory Periapical and Gingival Lesions. J Contemp Dent Pract 2014;15(3):300-305.


2017 ◽  
Author(s):  
Kathryn M. Lenz ◽  
Lindsay A. Pickett ◽  
Christopher L. Wright ◽  
Katherine T. Davis ◽  
Anabel Galan ◽  
...  

AbstractSex differences in brain and behavior are programmed during development by gonadal hormones. We found that the immune system-derived mast cell is a primary target for the masculinizing hormone, estradiol. Male rats had more mast cells in the preoptic area (POA), a brain region essential for male copulatory behavior, during the critical period for sexual differentiation. Activating mast cells in females masculinized POA neuronal and microglial morphology and adult sex behavior, and inhibiting mast cells in males blunted masculinization. Estradiol increased mast cell number and caused mast cells to release histamine, which stimulated microglia to release prostaglandins and thereby induced male-typical synaptic patterning. Inducing an allergic reaction in pregnant dams increased mast cell number in the brains of female fetuses and masculinized neuronal and microglia morphology and adult copulatory behavior. These findings identify a novel non-neuronal origin of brain sex differences and non-steroidal source of variability in brain feminization.


Blood ◽  
1994 ◽  
Vol 84 (8) ◽  
pp. 2489-2496 ◽  
Author(s):  
M Rottem ◽  
T Okada ◽  
JP Goff ◽  
DD Metcalfe

Abstract Mast cells may be cultured from human peripheral blood in the presence of recombinant human stem cell factor (rhSCF). The characteristics of the cells in peripheral blood that give rise to mast cells are unknown. Because mast cell precursors in human marrow are CD34+, human peripheral blood mononuclear cells from patients with mastocytosis and normal controls were sorted on the basis of CD34 expression and the positive and negative cell populations were cultured in rhSCF, recombinant human interleukin-3 (rhIL-3), or both for 6 weeks. Cell cultures were examined every 2 weeks for total and mast cell number and cell differential using Wright Giemsa and acid toluidine blue stains and antibodies to mast cell tryptase and chymase, cell-associated histamine, and expression of CD34, c-kit, Fc epsilon RI, and Fc gamma RII using flow cytometric analysis. The ultrastructural anatomy of mast cells was examined by electron microscopy. Peripheral blood CD34+ cells cultured in rhSCF with or without rhIL-3 gave rise to cell cultures consisting of greater than 80% mast cells by 6 weeks. CD34+ cells cultured in rhIL-3 alone did not give rise to mast cells, whereas rhIL- 3 plus rhSCF increased the final mast cell number eightfold when compared with cells cultured in rhSCF alone. Mast cells increased concomitantly with a decrease in large undifferentiated mononuclear cells. CD34- cells did not give rise to mast cells. Histamine content per cell at 6 weeks was approximately 5 pg. Electron microscopy of 4- week cultures showed immature mast cells containing predominantly tryptase-positive granules that were either homogeneous or contained lattice structures, partial scroll patterns, or central dense cores and mixtures of vesicles, fine granular material, and particles. The CD34+ population at day 0 expressed Kit (65%) and Fc gamma RII (95%), but not Fc epsilon RI, by fluorescence-activated cell sorter analysis. At 6 weeks, CD34+-derived mast cells exhibited Fc epsilon RI in addition to Kit and Fc gamma RII, and were negative for CD34 antigen. Patients with mastocytosis showed a higher number of mast cells per CD34+ cell cultured compared with normal controls. Thus, the mast cell precursor in human peripheral blood is CD34+/Fc epsilon RI- and gives rise to mast cells in the presence of rhSCF with or without rhIL-3, and the number of mast cells arising per CD34+ cell in culture is greater when the CD34+ cells are obtained from patients with mastocytosis compared with normal subjects.


Blood ◽  
1994 ◽  
Vol 84 (8) ◽  
pp. 2489-2496 ◽  
Author(s):  
M Rottem ◽  
T Okada ◽  
JP Goff ◽  
DD Metcalfe

Mast cells may be cultured from human peripheral blood in the presence of recombinant human stem cell factor (rhSCF). The characteristics of the cells in peripheral blood that give rise to mast cells are unknown. Because mast cell precursors in human marrow are CD34+, human peripheral blood mononuclear cells from patients with mastocytosis and normal controls were sorted on the basis of CD34 expression and the positive and negative cell populations were cultured in rhSCF, recombinant human interleukin-3 (rhIL-3), or both for 6 weeks. Cell cultures were examined every 2 weeks for total and mast cell number and cell differential using Wright Giemsa and acid toluidine blue stains and antibodies to mast cell tryptase and chymase, cell-associated histamine, and expression of CD34, c-kit, Fc epsilon RI, and Fc gamma RII using flow cytometric analysis. The ultrastructural anatomy of mast cells was examined by electron microscopy. Peripheral blood CD34+ cells cultured in rhSCF with or without rhIL-3 gave rise to cell cultures consisting of greater than 80% mast cells by 6 weeks. CD34+ cells cultured in rhIL-3 alone did not give rise to mast cells, whereas rhIL- 3 plus rhSCF increased the final mast cell number eightfold when compared with cells cultured in rhSCF alone. Mast cells increased concomitantly with a decrease in large undifferentiated mononuclear cells. CD34- cells did not give rise to mast cells. Histamine content per cell at 6 weeks was approximately 5 pg. Electron microscopy of 4- week cultures showed immature mast cells containing predominantly tryptase-positive granules that were either homogeneous or contained lattice structures, partial scroll patterns, or central dense cores and mixtures of vesicles, fine granular material, and particles. The CD34+ population at day 0 expressed Kit (65%) and Fc gamma RII (95%), but not Fc epsilon RI, by fluorescence-activated cell sorter analysis. At 6 weeks, CD34+-derived mast cells exhibited Fc epsilon RI in addition to Kit and Fc gamma RII, and were negative for CD34 antigen. Patients with mastocytosis showed a higher number of mast cells per CD34+ cell cultured compared with normal controls. Thus, the mast cell precursor in human peripheral blood is CD34+/Fc epsilon RI- and gives rise to mast cells in the presence of rhSCF with or without rhIL-3, and the number of mast cells arising per CD34+ cell in culture is greater when the CD34+ cells are obtained from patients with mastocytosis compared with normal subjects.


2009 ◽  
Vol 2009 ◽  
pp. 1-7 ◽  
Author(s):  
Ana Carolina Luchini ◽  
Déborah Mara Costa de Oliveira ◽  
Cláudia Helena Pellizzon ◽  
Luiz Claudio Di Stasi ◽  
José Carlos Gomes

The present study aimed to clarify the role of mast cells in colitis with relapse induced in Wistar rats by trinitrobenzenosulphonic acid. Colitis induction increased the histamine concentration in the colon, which peaked on day 26. The number of mast cells, probably immature, was ten times higher on day 8. Different from animals infected with intestinal parasites, after colitis remission, mast cells do not migrate to the spleen, showing that mast cell proliferation presents different characteristics depending on the inflammation stimuli. Treatment with sulfasalazine, doxantrazole, quercetin, or nedocromil did not increase the histamine concentration or the mast cell number in the colon on day 26, thereby showing absence of degranulation of these cells. In conclusion, although mast cell proliferation is associated with colitis, these cells and their mediators appear to play no clear role in the colitis with relapses.


2015 ◽  
Vol 459 (1) ◽  
pp. 131-136 ◽  
Author(s):  
Zhuo Zhao ◽  
Hao Wang ◽  
Marina Lin ◽  
Leanne Groban

Parasitology ◽  
1993 ◽  
Vol 106 (3) ◽  
pp. 297-304 ◽  
Author(s):  
T. Fujino ◽  
B. Fried ◽  
I. Tada

SUMMARYThe infectivity and distribution of Echinostoma trivolvis were studied in male, conventional and congenitally athymic nude mice, each infected with 30 metacercarial cysts. In conventional mice, worm recoveries at 6 and 8 days post-exposure were58·3 and 54·0%, respectively. Worm recovery declined to 44·0% by day 10, to 4·3% by day 13, and 0% by day 17. In athymic mice, worm recoveries at 6 and 8 days post-exposure were 61·7 and 36·3%, respectively. Worm recovery declined to 27·7% by day 10, to 0·7% by day 13, and 0% by day 17. The distribution of worms demonstrated a posteriad migration over time in both groups. Kinetic changes in the number of goblet and mucosal mast cells in the upper ileum of mice infected with E. trivolvis were examined. In conventional mice, the number of goblet cells increased rapidly to reach a peak at day 13 and then declined gradually. The number of goblet cells in athymic mice also increased to reach a peak at day 13, and then declined rapidly. However, the number of goblet cells in athymic mice was always less than that inconventional mice. The mast cell number in infected conventional mice increased rapidly to reach a peak at day 17 and then declined. There was no increase in the mast cell number of infected athymic mice throughout the experiment. Whereas common pathological changes occurred in the intestines of both mice groups infected with echinostomes some ultrastructural differences were observed in the gut epithelial cells of conventional versus athymic mice.


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