[Karyometric research on human lymph node cells. III. Basophil stem cells, plasma cells & tissue mast cells].
Explore the source record for details and available documents.
Basophils↗
SEARCH · PubMed Health
Results for “MAST CELLS”
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
[Morphological characteristics of human mast cells in normal and pathological thyroid glands. Functional aspect of human mast cells in comparison with rat mast cells].
We examined the distribution and population density of human mast cells in thyroid glands. The results were compared with those of Sprague-Dawley (SD) rats because they thyroid function of SD rats is known to be under the control of bioactive amines discharged from mast cells. Normal thyroid tissues were obtained either form autopsy or from a normal portion of the tissue distant from nodular lesions. Thyroid tissues were surgically removed from cases of Graves' disease and other tumorous lesions such as follicular adenoma, follicular carcinoma, papillary carcinoma and medullary carcinoma. The tissues were fixed with buffered formaldehyde or Carnoy fluid and embedded in paraffin. Mast cells were stained with toluidine blue and naphthol ASD chloroacetate esterase (esterase). Immunoperoxidase reactions to antihuman tryptase and chymase monoclonal antibodies were then observed. The mast cells were also observed by electron microscopy. The histamine content of the thyroid tissues was estimated by the high-performance liquid chromatography method. The mast cells in SD rat thyroid glands were scattered in perifollicular connective tissues which were comprised of capillaries, fibroblasts, nerve fibers and occasional fine deposits of collagen fibrils. Their cytoplasmic granules appeared to be distinct, electron dense and amorphous. In contrast, the mast cells in normal human thyroid glands were scattered exclusively over relatively thick interstitial spaces like the interlobular and subcapsular connective tissues. These mesenchymal tissues were composed of bundles of collagen fibrils, fibroblasts, histiocytes and thin cytoplasmic processes of unknown origin. In pathologic thyroid tissues, the mast cells were distributed in a similar pattern over the connective tissues.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
[Morphology and histochemistry of plasma cells and mast cells in breast tumors].
Explore the source record for details and available documents.
Adenofibroma↗
Mucosal mast cell responses and release of mast cell protease-I in infections of mice with Hymenolepis diminuta and H. microstoma: modulation by cyclosporin A.
The dynamics of intestinal mucosal mast cells and the major mucosal mast cell protease were followed during the course of laboratory infections of mice with Hymenolepis diminuta and H. microstoma. The effects of the drug cyclosporin A (CsA), which is both immunosuppressive and selectively anthelmintic depending upon dose regime, were determined. In H. diminuta infections worm expulsion occurred around day 9 and coincided with peak mastocytosis and peak mMCP-I concentrations in tissues and serum. Immunosuppressive treatment with CsA prevented worm expulsion, permitting some individuals to reach maturity, and abrogated mast cell proliferation and mMCP-I production and release. By contrast, H. microstoma infections persisted for 64 days in spite of a considerable mastocyosis in both intestine and bile duct tissues accompanied by a high level of mMCP-I in tissues and serum. A subimmunosuppressive regime of CsA had only limited effects on worms and mast cell numbers and activity. Together these data shed light on the variable mast cell response to gastrointestinal infections and on the potential significance of parasite location in evasion of mast cell action. Use of CsA reveals the contributions of both T cell-dependent mechanisms, including mast cell proliferation and activation, and T cell-independent events in regulating intestinal helminth infections.
Animals↗
Gene expression and regulation of nerve growth factor in atopic dermatitis mast cells and the human mast cell line-1.
The gene expression and regulation of nerve growth factor (NGF) in atopic dermatitis (AD) and the human mast cell line (HMC)-1 was investigated at the molecular level. NGF-stimulation of HMC-1 cells resulted in increases in tryptase activity and histamine contents, paralleled by an increase of tryptase and histamine at the transcriptional level. Also, an increased expression of NGF was found in AD lesions, in association with increased systemic NGF plasma levels. Further cutaneous sources for increased NGF levels were keratinocytes and fibroblasts. These findings demonstrate an increased expression of NGF in AD and effects on tryptase and histamine. Mast cells may be major mediators of neurotrophin effects in AD.
Cells, Cultured↗
Evidence for morphologic diversity of human mast cells. An ultrastructural study of mast cells from multiple body sites.
The ultrastructural features of 502 mast cells, including 34,187 granules, were studied from seven human tissue sites (lung, skin, colon, stomach, small bowel, breast parenchyma, and axillary lymph nodes). Granule areas and substructure were detailed according to the microenvironment (lung alveoli, lung bronchi, bowel mucosa, bowel submucosa, breast skin, breast parenchyma, and axillary lymph nodes). Although completely closed, discrete scrolls were present in some mast cell granules at all tissue locations, they were present more frequently in granules from bowel mucosa and lung (scroll-rich morphology). In contrast, most of the mast cell granules from skin, breast parenchyma, axillary lymph nodes, and bowel submucosa were rimmed by incomplete scrolls forming parallel lamellae; centrally, amorphous granular material and/or grating/lattice-like structures occurred (scroll-poor morphology). In breast, the latter granules had a mean granule area almost twice that of all other sites. Individual mast cells having granules with both scroll-rich and scroll-poor features were common in all tissue sites and microenvironments. In fact, 7.8% of mast cells had granules showing at least one completely closed, discrete scroll and grating/lattice-like structures, sometimes within the same granule. These observations indicate that mixed forms occur and that there is considerable morphologic diversity between the predominant mast cell found in mucosa and lung (scroll-rich morphology) and the predominant mast cell found in skin, breast parenchyma, axillary lymph nodes, and bowel submucosa (scroll-poor morphology).
Breast↗
Transforming growth factor-beta 1 selectively inhibits IL-3-dependent mast cell proliferation without affecting mast cell function or differentiation.
Transforming growth factor-beta 1 (TGF-beta 1) is an important regulator of cell growth, differentiation, and function. We show that TGF-beta 1 selectively inhibits IL-3-dependent mouse bone marrow derived mast cell (MBMMC) proliferation without affecting MBMMC function or differentiation. TGF-beta 1 significantly decreased [3H]thymidine uptake by IL-3-dependent MBMMC in a dose-dependent manner with 50% inhibition of proliferation occurring with a TGF-beta 1 concentration of 0.1 ng/ml. A brief (i.e., 30 min) incubation of MBMMC with TGF-beta 1 is sufficient to inhibit IL-3-induced proliferation of MBMMC (cultured in the absence of TGF-beta 1) for 24 to 48 h. The inhibitory effect of TGF-beta 1 on the IL-3-dependent proliferation of MBMMC is not cytotoxic as evident from the absence of MBMMC trypan blue staining, the retained functional characteristics of the MBMMC cultured in TGF-beta 1, and the reversibility of the TGF-beta 1 induced inhibition of IL-3 dependent MBMMC proliferation. MBMMC grown in TGF-beta 1 acutely (24 to 48 h) or chronically (7 to 14 days) do not exhibit functional differences in performed or newly generated mediator secretion (Ag/IgE or calcium ionophore A23187 induced MBMMC beta-hexosaminidase or leukotriene C4 release) from MBMMC grown in the absence of TGF-beta 1. In addition, MBMMC cultured for 2 wk in TGF-beta 1 do not show evidence of differentiation as assessed by cellular histamine content or Alcian blue/safranin staining. Thus, TGF-beta 1 is an important negative regulator of IL-3-dependent mast cell proliferation in vitro, selectively inhibiting IL-3-dependent MBMMC proliferation without affecting MBMMC function or differentiation.
Animals↗
In vitro inhibitory effect of rupatadine on histamine and TNF-alpha release from dispersed canine skin mast cells and the human mast cell line HMC-1.
OBJECTIVE AND DESIGN: To examine the inhibitory potential of rupatadine, a new H1-antihistamine and anti-PAF agent, on histamine and TNF-alpha release. Comparison with an H1-antihistamine (loratadine) and a PAF-antagonist (SR-27417A). MATERIAL: Dispersed canine skin mast cells were used to assess the effect of the drugs tested on FcepsilonRI-dependent and -independent histamine release; the human HMC-1 cell line was used to study TNF-alpha release. TREATMENT AND METHODS: Before stimulation mast cell populations were treated with increasing concentrations of rupatadine, loratadine and SR-27417A. Histamine and TNF-alpha release were measured following 15-30 min and 3 h activation, respectively. RESULTS: The IC50 for rupatadine in A23187, concanavalin A and anti-IgE induced histamine release was 0.7+/-0.4 microM, 3.2+/-0.7 microM and 1.5+/-0.4 microM, respectively whereas for loratadine the IC50 was 2.1+/-0.9 microM, 4.0+/-1.3 M and 1.7+/-0.5 microM. SR-27417A exhibited no inhibitory effect. Rupatadine, loratadine and SR-27417A inhibited TNF-alpha release with IC50 2.0+/-0.9 microM, 2.1+/-1.1 M and 4.3+/-0.6 microM, respectively. CONCLUSIONS: Rupatadine and loratadine showed similar inhibitory effect on histamine and TNF-alpha release, whereas SR-27417A only exhibited inhibitory effect against TNF-alpha.
Animals↗
3T3 fibroblasts induce cloned interleukin 3-dependent mouse mast cells to resemble connective tissue mast cells in granular constituency.
As assessed by ultrastructure, histochemical staining, and T-cell dependency, in vitro-differentiated inter-leukin 3-dependent mouse mast cells are comparable to the mast cells that reside in the gastrointestinal mucosa but not in the skin or the serosal cavity of the mouse. We now demonstrate that when cloned interleukin 3-dependent mast cells are cocultured with mouse skin-derived 3T3 fibroblasts in the presence of WEHI-3 conditioned medium for 28 days, the mast cells acquire the ability to stain with safranin, increase their histamine content approximately equal to 50-fold and their carboxypeptidase A content approximately equal to 100-fold, and augment approximately equal to 45-fold their biosynthesis of proteoglycans bearing 35S-labeled heparin relative to 35S-labeled chondroitin sulfate glycosaminoglycans. Thus, fibroblasts induce interleukin 3-dependent mouse mast cells to change phenotype from mucosal-like to connective tissue-like, indicating that the biochemical and functional characteristics of this mast cell type are strongly influenced by the connective tissue microenvironment.
Animals↗
IL-4 modulates the histamine content of mast cells in a mast cell/fibroblast co-culture through a Stat6 signaling pathway in fibroblasts.
IL-4 plays a crucial role in the pathogenesis of allergic diseases, such as the induction of IgE synthesis and the development of mast cells. To further understand the effect of IL-4 on mast cells in skin, we utilized a mast cell/fibroblast co-culture system as an in vitro model of dermal mast cells. IL-4 induced mast cell growth in the culture with fibroblasts. Immunoblot analysis revealed that IL-4 activated Stat6 in both mast cells and fibroblasts. The over-expression of dominant-negative Stat6 in fibroblasts in the presence of IL-4 decreased the histamine content per mast cell, but not the number of mast cells. In contrast, the over-expression of constitutively-active Stat6 in fibroblasts increased the histamine content per mast cell, indicating that the activation of Stat6 in fibroblasts supports the maturation of mast cells co-cultured with fibroblasts.
3T3 Cells↗
Significance of tissue chromaffin cells and mast cells in man.
Explore the source record for details and available documents.
Chromaffin Cells↗
A novel cell-to-cell interaction between mast cells and other cell types.
Time-lapse cinephotomicrography and transmission electron microscopy (TEM) have been used to study the interactions between rat mast cells and different cell monolayers in culture (fibroblasts, vascular endothelial cells and cardiac muscle cells). This report documents a novel form of behavior between mast cells and certain other cell types. We have tentatively termed this cellular behavior 'transgranulation', which involves sequential changes not seen in control cells, including: (1) formation of a granule-containing mast cell pseudopod that becomes closely applied to an adjacent cell; (2) development of specialized plasma membrane interrelationships between apposing cells; (3) alteration of granules and perigranular membranes within the mast cell pseudopod; (4) occasional transfer of exocytosed mast cell granules to the cytoplasm of the adjacent cell; (5) presence of a specialized inclusion body in the mast cell; and finally, (6) either withdrawal of the pseudopod by the mast cell, or casting-off of the pseudopod from the mast cell, leaving it on the surface of the adjacent cell (pseudopod translocation). These mast cell interactions occur specifically with fibroblasts and endothelial cells in vitro and are never observed with cardiac muscle cells or non-cellular substrates. Our investigations of rat mesenteries in situ confirm that these cell-cell interactions also occur in vivo. We suggest it represents a form of cell-to-cell communication involving secretion from a mast cell pseudopod to another cell type. The significance of specialized contacts between mast cells and other cell types in vivo is discussed.
Animals↗
Leukemic cell membrane from acute myelogenous leukemias with massive mast cell infiltration has a mast cell differentiation activity under culture condition containing interleukin 3.
Five cases of acute myelogenous leukemia with massive mast cell infiltration in bone marrow and leukemic tumors of the soft tissue were examined to elucidate the relationship between leukemic cells and mast cells. Leukemic cells in each case showed no basophil/mast cell features and differentiated to neutrophil-like cells in liquid culture. Isolated mast cells failed to proliferate with or without growth factors used irrespective of culture conditions. Mononuclear cell fraction obtained from all patients gave rise to relatively numerous mast cells in interphase culture using IL-3 but not in other culture systems. The simultaneous addition of leukemic cell membrane and IL-3 or delayed addition of leukemic cell membrane produced more numerous and mature mast cells in the upper layer of interphase culture using IL-3. However, addition of leukemic cell membrane alone failed to increase the number of mast cells. Similar results were obtain using mononuclear cells obtained from volunteers and cord blood cells. These results indicate that a cell to cell contact or interstitial substance together with IL-3 are essential requirements for growth and maturation of mast cell precursors and that the cell membrane itself in some cases of leukemia has the ability to induce maturation of mast cell precursors.
Adolescent↗
Separation of lymphocytes and mast cells from the Furth transplantable mast cell tumor in an isokinetic gradient of Ficoll in tissue culture medium.
Cell suspensions of the transplantable Furth murine mast cell tumor were separated both by velocity sedimentation in an isokinetic gradient and by isopyknic sedimentation. Prior to separation, the suspension of tumor cells contained 60.3+/-13.1% (S.D.) malignant mast cells, 9.8+/-10.4% lymphocytes, 4.3+/-2.1% granulocytes, 1.7+/-1.9% macrophages, 0.6+/-0.4% unidentified cells, and 22.8+/-8.5% red blood cells. After either isokinetic or isopyknic sedimentation, more than 97% of the nucleated cells in the purest modal fraction were malignant mast cells. Velocity sedimentation in the isokinetic gradient offered several advantages over isopyknic separation of this tumor; namely, in isokinetic sedimentation, the cells are exposed to a lower centrifugal force for a shorter period of time; a much larger proportion of mast cells were in the highly purified zone of the gradient following velocity sedimentation; and lymphocytes were more highly purified (88.9+/-10.1% of the nucleated cells) following velocity sedimentation. Granulocytes and macrophages were purified more than 8-fold over the nucleated cells in the starting sample suspension. The purified cells from this tumor offer the opportunity to study the interactions between highly purified, easily identified, malignant cells and cells that may participate in the defense of the host against cancer.
Cell Separation↗
Human mast cell heterogeneity: histamine release from mast cells dispersed from skin, lung, adenoids, tonsils, and colon in response to IgE-dependent and nonimmunologic stimuli.
We have compared the ability of anti-IgE, calcium ionophore A23187, substance P, compound 48/80, poly-L-lysine, and morphine to release histamine from mast cells of human skin, lung, adenoids, tonsils, and colon. Use of a single collagenase/hyaluronidase dispersion technique for all tissues has allowed comparisons of reactivity to be made that are free from methodological variations. Mast cells from all tissues examined secreted histamine in response to anti-IgE and calcium ionophore A23187. However, only skin mast cells were responsive to substance P, compound 48/80, poly-L-lysine, and morphine. Activation of human skin mast cells by these nonimmunologic stimuli clearly distinguishes them from the mast cells of human lung, adenoids, tonsils, and colon and is indicative of functional heterogeneity within the human mast cells population. We propose that the presence of functional receptor sites for neuropeptides and basic compounds on skin mast cells that are not present in mast cell populations from mucosal or lymphoid sources reflects a specialized role for these cells in vascular homeostasis.
Adenoids↗
KIT mutation in mast cells and other bone marrow hematopoietic cell lineages in systemic mast cell disorders: a prospective study of the Spanish Network on Mastocytosis (REMA) in a series of 113 patients.
Despite the relevance of the c-kit/stem cell factor (SCF) signaling pathway in mast cell (MC) diseases, the exact frequency of KIT mutations in different compartments of bone marrow (BM) hematopoietic cells of individuals with systemic mastocytosis (SM), and its different diagnostic categories, remains unknown. In this study, we prospectively analyzed the presence of KIT mutations in fluorescence-activated cell-sorting (FACS)- purified populations of BM MCs (n = 113) and other BM cell compartments (n = 67) from adults with SM. Our results show the presence of D816V KIT mutation in virtually all adults (93%) with indolent and aggressive forms of SM, except well-differentiated SM (29%), while other KIT mutations were rarely (< 3%) detected. In around one-third of patients with mutated MCs, the KIT mutation was also detected in CD34+ hematopoietic cells and eosinophils, and, to a lesser extent, in monocytic, neutrophil-lineage BM precursor cells and lymphocytes. Most patient with poor-prognosis SM (81%) carried the KIT mutation in 2 or more BM myeloid cell populations, while this was detected in a smaller proportion (27%) of indolent cases. These results would support the notion that KIT mutation is a hallmark of adult SM where it targets a pluripotent hematopoietic stem cell, and may contribute to explaining previously observed discrepancies in the literature.
Adolescent↗
Migration of stromal cells supporting mast-cell differentiation into open wound produced in the skin of mice.
Mutant mice of Sl/Sld genotype are depleted of tissue mast cells due to a defect of stromal cells which may support the differentiation of mast cells. Number of mast cells did not increase in the skin of Sl/Sld mice grafted on the back of the congenic +/+ mice even 50 weeks after the transplantation. When the wound was produced in the central part of the Sl/Sld skin graft, a considerable number of mast cells appeared within the scar resulting from the wound. The appearance of mast cells in the scar was shown to be due to the differentiation of circulating precursors into mast cells rather than the simple migration of mature mast cells by using giant granules of bgJ/bgJ mice as a marker for newly-formed mast cells. Therefore, the present results seem to suggest that normal stromal cells of the +/+ host origin migrate into the wound produced in the grafted skin of Sl/Sld mice and support the differentiation of circulating precursors into mast cells.
Anemia, Macrocytic↗
Levels of mast-cell growth factors in plasma and in suction skin blister fluid in adults with mastocytosis: correlation with dermal mast-cell numbers and mast-cell tryptase.
BACKGROUND: Mast-cell accumulation has been observed in the skin and other organs of patients with systemic indolent mastocytosis (SM). The basis for this pathologic increase is not fully understood. OBJECTIVE: We sought to determine levels of mast-cell growth factors in the skin and plasma of patients with SM, patients with atopic dermatitis (AD), and healthy individuals and to correlate these levels to dermal mast-cell numbers and levels of mast-cell tryptase. METHODS: Skin suction blister fluid and plasma levels of stem-cell factor, IL-3, IL-4, IL-6, vascular endothelial growth factor, and total mast-cell tryptase were analyzed by means of ELISA. The number of mast cells was determined in a biopsy section taken from adjacent skin. RESULTS: Mast-cell numbers in the dermis were higher in patients with SM compared with numbers in patients with AD (P <.001) or in healthy control subjects (P <.0001) and correlated with tryptase levels in both skin blister fluid (P <.0001) and plasma (P <.0001). Stem-cell factor and vascular endothelial growth factor levels in the skin blister fluid and plasma of patients with SM were not significantly different from those in patients with AD or healthy control subjects. IL-3 and IL-4 levels were below the limit of detection. IL-6 levels were significantly increased in the plasma of patients with SM compared with in plasma of patients with AD (P <.002) and healthy control subjects (P <.0001) and correlated with plasma tryptase levels (P <.05) and dermal mast-cell numbers (P <.02). CONCLUSION: Because elevated levels of IL-6 could contribute to the fever, fatigue, and osteoporosis observed in patients with SM and because IL-6 is antiapoptotic for mast cells, IL-6 could potentiate the biologic consequences of this disease.
Adult↗