Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of IPD-1151T (suplatast tosilate), a novel anti-allergic drug, on murine mast cell induction were examined by the in vitro cell culture technique. Spleen cells from BALB/c mice suspended in RPMI-1640 medium containing interleukin 3 were cultured in the presence or absence of IPD-1151T. Half the volume of the medium was changed every 4 days. Mast cell numbers increased as the culture time went on and reached a peak on the 16th day, when spleen cells were cultured without IPD-1151T. However, induction of mast cells from spleen cell cultures was inhibited by IPD-1151T in a dose dependent fashion. These results strongly suggest that IPD-1151T is a very useful agent for therapy in allergic diseases.
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PMID:[Inhibitory effect of IPD-1151T (suplatast tosilate) on mast cell induction from normal mouse spleen cells]. 133 62

A simple method is described for the preparation of large numbers of mast cells from mouse spleen cells in vitro. Mouse spleen cells were cultured with RPMI 1640 medium supplemented with 10% FCS and 2-ME. Half of the total volume of the medium was changed every 4-5 days. Mast cell numbers increased with the culture time and reached a peak between 16 and 20 days. Using this method, 2 x 10(6) mast cells could be induced from 1 x 10(7) nucleated normal spleen cells. T cells and supernatant derived from ConA-stimulated T cells were unnecessary for mast cell induction. Phenotype analysis by FACS showed that Thy1,2, L3T4, Ly-2, Ig, B220, Asialo GM1, and WGA receptors were all negative but functional IgE receptors were positive. The granules in the cells could be stained by alcian blue but not by safranin. There was 1.632 +/- 0.024 micrograms stored histamine in 1 x 10(6) of the cells. Histamine was released from the cells in an antigen-induced and IgE-mediated process. Compound 48/80 and A23187 induced degranulation of the cells, and the mast cells were able to respond to ConA.
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PMID:Induction and identification of mast cells from long-term culture of mouse spleen cells without conditioned medium. 137 14

Mouse bone marrow hematopoietic stem cells were isolated from mouse femur bone and cultured in RPMI 1640 supplemented medium with 20 units/ml of the purified T-cell lymphokine, interleukin 3 (IL-3), IL-3 was uniquely able to induce the proliferation and differentiation of mature mast cells in vitro. The sparse granulation of the bone marrow-derived mast cells (BMMC) can be seen by day 5, progressing to definable mast cells by day 7, the mast cells appear morphologically mature and comprise a 96% pure population after 14 days of the culture. The monocytes macrophages, eosinophils and neutrophils disappeared by day 9. After 4 weeks of tissue culture, mast cells are fully mature and completely granulated at 98% cell purity. The BMMC are mononuclear, oval or round in shape and appear smaller than rat peritoneal mast cells. BMMC are stable over 3-5 months in conditioned medium. The homogeneous mast cell population possesses membrane receptors and mediators, such as histamine in their metachromatic granules. The histamine content of BMMC in culture between 2 to 4 weeks rose from 1.43 to 1.82 pg/cell. Moreover, the percentage of histamine release caused by 0.1 microM and 1.0 microM ionophore A23187 was 15% and 35%, respectively. By contrast, the histamine releasing activity of 0.01% and 0.001% compound 48/80 were 12 +/- 2% and 59 +/- 7% respectively. The granular density, histamine content and histamine release activity of BMMC are different from that of peritoneal mast cells.
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PMID:Effect of interleukin 3 on the differentiation and histamine content of cultured bone marrow mast cells. 170 84

Although mast cells and interferons are both involved in numerous immune and inflammatory responses, little is known about how microenvironmental factors such as interferons (IFNs) influence mast cell function. To study this question, sensitized peritoneal mast cells (greater than 98% purity) obtained from rats infected 4 weeks earlier with the parasite Nippostrongylus brasiliensis were preincubated for 24 hr with rat IFN-alpha/beta in RPMI-1640, then stimulated to degranulate with worm antigens. In the absence of antigen, IFN-alpha/beta had no noticeable effect on histamine release. However, in the presence of antigen, IFN-alpha/beta (150-1500 U/ml) inhibited histamine release in a dose-dependent manner (22.2 +/- 7.5% to 56.3 +/- 6.9%, n = 10). This inhibitory effect was neither heat (56 degrees for 1 hr) nor acid (pH 2 for 18 hr) labile, but was completely blocked by anti-IFN antibodies. In the presence of compound 48/80 (1 microgram/ml) or substance P (5 X 10(-5) M), IFN-alpha/beta was ineffective at modulating histamine release. Histamine release induced by antigen in the presence of the membrane phospholipid phosphatidyl-serine (30 micrograms/ml) was inhibited by IFN in a dose-dependent manner, but maximal inhibition (25.3 +/- 2.7%, n = 10) was reached at a lower concentration of IFN (750 U/ml) than when antigen was used alone. Therefore, rat IFN-alpha/beta appears to inhibit histamine release from rat mast cells in a dose- and stimulus-dependent manner and may do so by reducing the fluidity of the cell membrane.
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PMID:Interferon-alpha/beta inhibits IgE-dependent histamine release from rat mast cells. 246 45

The influence of IPD-1151T (suplatast-tosilate) on murine mast cell induction was examined by in vitro cell culture. Splenocytes from BALB/c mice suspended in RPMI-1640 medium supplemented with interleukin-3 were cultured in the presence or absence of IPD-1151T. Half of the total volume of the medium was changed every 4-5 days. The number of mast cells increased with culture time and reached a peak on the 16th day when the cells were cultured without IPD-1151T. However, the growth of mast cells from the splenocyte culture was dose dependently inhibited by IPD-1151T. Furthermore, IPD-1151T inhibited the proliferation of mast cell progenitor cells, IC-2, but not that of splenocytes or mature mast cells.
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PMID:Suppressive effects of IPD-1151T (suplatast-tosilate) on induction of mast cells from normal mouse splenocytes. 795 88

A method for cell purification was designed without using high-density media which may impair membrane receptors. Rat and mouse mast cells were separated with an improved nonsynchronous flow-through coil planet centrifuge. Peritoneal cells were suspended at a concentration of 2-3x10(7) cells/ml in conditioned RPMI 1640, supplemented with 50% heat-inactivated FCS and 0.32% sodium citrate. In each separation 3 ml of cell suspension were loaded into the coiled column and elutriated at 4 degrees C. Several conditions, including the centrifugal force, revolution/rotation ratio, density of separation media, flow speed, and designs of both coiled column and flow tubes, were examined and optimized for mast cell purification. Rat mast cells were separated at the purity of 99.2%, with an average yield of 40% under sterile conditions. Nearly 90% pure mouse mast cells were harvested, despite a very low population of mast cells available in murine peritoneal cells. Purified cells were morphologically intact and discharged granules by exocytosis as indicated by electron-microscopic observations. The average histamine release with antigenic specificity was 34 and 61%, in passive sensitization in vitro and in vivo, respectively. Mast cells sensitized with mouse monoclonal IgE antibody released histamine, similar to cells sensitized with homologous antibody. This newly devised method of cell separation will be useful to purify biologically intact mast cells.
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PMID:Purification of mast cells with an improved nonsynchronous flow-through coil planet centrifuge. 863 23

Arum maculatum agglutinin (AMA) is a monocot lectin isolated from tubers of Arum maculatum L. (Araceae) which exhibits different specificity towards oligo-mannosidic-type and N-acetyllactosaminic-type glycans. We have investigated the effect of this lectin on the cells of the immune system. Models of neutrophil migration in vivo, neutrophil chemotaxis in vitro and macrophage cultures were used to study the lectin inflammatory activity. When administered into rat peritoneal cavities, AMA (80, 200 and 500 microg/mL/cavity) induced significant and dose-dependent neutrophil migration. This effect was inhibited by incubation with alpha-methyl-d-mannoside. A 83% depletion in the number of resident cells following peritoneal lavage did not reduce the AMA-induced neutrophil migration, as compared to sham animals (not washed). However, pre-treatment with 3% thioglycolate which increases the peritoneal macrophage population by 236%, enhanced the neutrophil migration induced by AMA (200 microg/mL/cavity) (119%, p < 0.05). Reduction of peritoneal mast cell population by chronic treatment of cavities with compound 48/80 did not modify AMA-induced neutrophil migration. The neutrophil chemotaxy assay in vitro shows that the lectin (300 microg/mL) induces neutrophil chemotaxy (368% p < 0.05) compared to RPMI. Finally, injection into peritoneal cavities of supernatants from macrophage cultures obtained after stimulation with AMA (300 microg/mL) enhanced neutrophil migration (110% p < 0.05). Summarizing, our data suggest that A. maculatum agglutinin presents pro-inflammatory activity, inducing neutrophil migration by two ways, one which is independent on resident cells and another one dependent on the presence of these cells.
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PMID:Pro-inflammatory effect of Arum maculatum lectin and role of resident cells. 1591 76