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PubMed1994

Comparative cytokine release from human monocytes, monocyte-derived immature mast cells, and a human mast cell line (HMC-1).

To obtain further information regarding the role of cytokines during mast cell differentiation, we have investigated changes of cytokine secretion in mast cells developing from the human peripheral blood monocytic cell fraction during culture with fibroblast-derived conditioned media. The influence of stem cell factor and an antibody to the respective receptor in our culture system was studied as well. Interleukin (IL)-1 alpha, IL-1 beta, IL-6, and tumor necrosis factor (TNF)alpha were spontaneously secreted by cultured cells at day 1 and decreased markedly by day 14. Similar changes occurred also during culture with stem cell factor and were partially abrogated by an anti-receptor antibody. IL-8 was secreted at a high level throughout the culture, whereas no spontaneous secretion of IL-2, IL-3, IL-4, and IL-7 was measured at all. Upon stimulation with phorbol myristate acetate and A23187, cultured cells showed substantially more release of IL-3 and TNF-alpha after 14 d of culture, compared to peripheral blood monocytic cells. Preformed TNF-alpha was found in one of three monocytic cell preparations from peripheral blood, but not in monocytic cell-derived mast cells. During mast cell differentiation, cytokines from monocytic cells are therefore downregulated while the cells assume a pattern typically found in mast cells.

Cell Line↗
PubMed1999

ICAM-3 (CD50) is expressed by human mast cells: induction of homotypic mast cell aggregation via ICAM-3.

Intercellular adhesion molecule-3 (ICAM-3, CD50), an adhesion receptor of the immunoglobulin superfamily, is suggested to play a key role in adhesive cellular interactions during the initial phase of an immune response. We here provide evidence that ICAM-3 is abundantly expressed by cells of the human mast cell line HMC-1 and, to a lower degree, by purified skin mast cells, as demonstrated by flow-cytometry, ELISA and RT-PCR. ICAM-3 immunoprecipitated from surface biotinylated HMC-1 cells migrates as a broad band of Mr 124,000 by Western blot analysis. We also demonstrate that monoclonal antibodies directed against ICAM-3 are capable of inducing rapid HMC-1 cell aggregation, the extent of which strongly depends on the epitope recognized by the mAb applied. Interestingly, although inhibitable by two of six mAbs against LFA-1, HMC-1 aggregation induced via ICAM-3 appears to be mediated by an adhesive pathway independent of LFA-1. Dermal mast cells are also aggregated with anti-ICAM-3 mAbs, a phenomenon which has not been described before for isolated tissue mast cells. However, this process displays slower kinetics, as compared to HMC-1 cells. That anti-ICAM-3 mAbs are able to mediate biological effects is further illustrated by their capability to increase stimulation-dependent release of the pro-inflammatory cytokines interleukin-6 (IL-6) and IL-8 from HMC-1 cells. Taken together, these results indicate that ICAM-3 is not only expressed by immature and mature human mast cells, but also possesses functional relevance and may therefore play a significant role in mast cell associated processes.

Animals↗
PubMed2000

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

OBJECTIVE: To determine whether human testicular mast cells contain the potent fibroblast growth factor tryptase and to examine changes in mast cell morphology and intratesticular distribution in testes with normal spermatogenesis versus abnormal spermatogenesis. DESIGN: Retrospective evaluation of testicular biopsies with the use of immunohistochemistry, morphometry, and electron microscopy. SETTING: University research and clinical institutes. PATIENT(S): Infertile men (total of 24) with severe hypospermatogenesis, germ cell arrest syndrome, or Sertoli cell only syndrome, and men without pathologies. INTERVENTION(S): Diagnostic testicular biopsy. MAIN OUTCOME MEASURE(S): Location, number, and distribution of testicular mast cells. RESULT(S): All groups showed tryptase-positive mast cells. In specimens with normal spermatogenesis, mast cells were round and located mainly in the interstitial spaces close to Leydig cells. In germ cell arrest syndrome, a 2-fold increase was evident, and in Sertoli cell only syndrome, a >3-fold increase of tryptase-immunoreactive mast cells became evident. Moreover, there was a statistically significant shift of the cells from the interstitium to the tubular walls in Sertoli cell only syndrome and germ cell arrest syndrome. Mast cells in specimens of Sertoli cell only syndrome and germ cell arrest syndrome were heterogeneous, with rounded or elongated shapes and signs of degranulation. The thickness of the tubular walls was doubled in specimens of germ cell arrest syndrome and Sertoli cell only syndrome in comparison with normal specimens, and this increase was positively correlated with the number of mast cells in these patients. CONCLUSION(S): Our results suggest that mast cell products, including the potent fibroblast growth factor tryptase, are involved in the thickening of the tubular wall and other changes in infertile testes.

Adult↗
PubMed1998

Comparative morphofunctional study of dispersed mature canine cutaneous mast cells and BR cells, a poorly differentiated mast cell line from a dog subcutaneous mastocytoma.

The dog mastocytoma BR cell line provides us with a permanent source of canine mast cells, allowing a characterization of secretory mediators that exert important effects in canine allergic and nonallergic diseases and in physiological processes. We studied the ultrastructural characteristics and histamine releasing activity after immunological and non-immunological stimuli of the dog mastocytoma BR cell line, and compared the cell line to normal skin mast cells enzymatically isolated from healthy dogs. The histamine content of BR cells was 0.04 +/- 0.002 pg/cell, approximately 100-fold less than that found in canine skin mast cells. Non-immunologic stimuli induced similar concentration-dependent histamine release from skin mast cells and BR cells: 29.3 +/- 0.9% vs. 12.7 +/- 0.7% (calcium ionophore A23187), 23.3 +/- 0.7% vs. 18.8 +/- 0.7% (substance P) and 12.5 +/- 0.3% vs. 12.1 +/- 0.9% (compound 48/80), respectively. Immunologic stimulation, however, was only effective on canine skin mast cells, causing 30.9 +/- 1.7%, 27.7 +/- 0.6% and 12.2 +/- 0.9% histamine release in response to anti-canine IgE, concanavalin A, and antigen Asc S 1, respectively. The absence of functional IgE receptors in BR cells was confirmed by the lack of response to anti-IgE and antigen Asc S 1 following passive sensitization with dog atopic serum and dog antigen sensitized serum. We conclude that BR cells are able to release histamine after non-immunologic stimulation in a similar manner to canine skin mast cells, but that there are morphological and functional differences possibly due to different states of maturity or differentiation. For this reason the study of the highly homogeneous BR cells could offer insights into dog mast cell biology in contexts where freshly isolated cells cannot be used because of low purity and recovery.

Animals↗
PubMed1994

Lack of expression of the tryptase mouse mast cell protease 7 in mast cells of the C57BL/6J mouse.

Although the steady-state level of the mouse mast cell protease (mMCP) 7 transcript is below detection in the serosal and mucosal mast cells of the BALB/cJ mouse, the IL-3-dependent, bone marrow-derived mast cells (mBMMC) of this strain and four other strains contain a high steady-state level of the mMCP-7 transcript. To further analyze the expression of this mast cell tryptase, a mMCP-7-specific IgG was obtained by immunizing a rabbit with a 19-residue synthetic peptide that corresponds to its unique amino acid sequence at residues 160 to 178 (anti-mMCP-7(160-178). In a SDS-PAGE/immunoblot analysis of lysates of BALB/cJ mBMMC, anti-mMCP-7(160-178) IgG recognized a diffuse 31- to 36-kDa protein, which shifted to a sharp 27-kDa protein after treatment with N-glycanase. As assessed immunohistochemically, mMCP-7 protein is present not only in the secretory granules of BALB/cJ mBMMC, but also in the ear mast cells of this strain. In contrast, the ear mast cells of the C57BL/6J mouse do not contain detectable levels of mMCP-7 protein, although the ear mast cells of both mouse strains contain mMCP-5 protein. Because mMCP-7 mRNA and protein also were not detected in mBMMC from the C57BL/6J mouse, the failure of the ear mast cells of this strain to express mMCP-7 is most likely a consequence of an intrinsic abnormality in the mast cell-committed progenitor cells themselves, or in the bone marrow microenvironment that induces its mast cell progenitor cells to express this tryptase.

Amino Acid Sequence↗
PubMed1992

Inflammatory responses in the intestine during tapeworm infections. Mucosal mast cells and mucosal mast cell proteases in Sprague-Dawley rats infected with Hymenolepis diminuta.

Comparative studies were made of two populations of Sprague-Dawley rats infected with Hymenolepis diminuta. The time course of infection, the development of mucosal mastocytosis and the levels of rat mucosal mast cell (MMC) protease (RMCP II) in serum and in jejunal mucosal tissues were monitored at intervals after infection with 40 cysticercoids of the tapeworm. Worm expulsion patterns differed markedly between the two populations, rats of New Zealand origin showing an abrupt and clear-cut loss of worms, rats of English origin showing a more gradual decline over a longer time period. In both populations, however, numbers of MMC and levels of tissue RMCP II were positively correlated with time after infection and negatively correlated with worm numbers. In only one of the three experiments (using English strain rats over a short time period) did levels of serum RMCP II change with time. In the other two experiments, in which English-strain and New Zealand-strain rats were used, there were no correlations between serum RMCP II and time, numbers of MMC, numbers of worms or levels of tissue RMCP II. The absence of correlation between serum RMCP II and worm loss in these experiments implies that MMC have no direct role in expulsion of H. diminuta. The data do show, nevertheless, that this purely luminal tapeworm is fully capable of activating the mucosal T lymphocyte-MMC precursor axis to elicit a mucosal mastocytosis.

Animals↗
PubMed1997

Transcription factor GATA-2 is required for proliferation/survival of early hematopoietic cells and mast cell formation, but not for erythroid and myeloid terminal differentiation.

The zinc-finger transcription factor GATA-2 plays a critical role in maintaining the pool of early hematopoietic cells. To define its specific functions in the proliferation, survival, and differentiation of hematopoietic cells, we analyzed the hematopoietic potential of GATA-2-/- cells in in vitro culture systems for proliferation and maintenance of uncommitted progenitors or differentiation of specific lineages. From a two-step in vitro differentiation assay of embryonic stem cells and in vitro culture of yolk sac cells, we demonstrate that GATA-2 is required for the expansion of multipotential hematopoietic progenitors and the formation of mast cells, but dispensable for the terminal differentiation of erythroid cells and macrophages. The rare GATA-2-/- multipotential progenitors that survive proliferate poorly and generate small colonies with extensive cell death, implying that GATA-2 may play a role in both the proliferation and survival of early hematopoietic cells. To explore possible mechanisms resulting in the hematopoietic defects of GATA-2-/- cells, we interbred mutant mouse strains to assess the effects of p53 loss on the behavior of GATA-2-/- hematopoietic cells. Analysis of GATA-2-/-/p53-/- compound-mutant embryos shows that the absence of p53 partially restores the number of total GATA-2-/- hematopoietic cells, and therefore suggests a potential link between GATA-2 and p53 pathways.

Animals↗
PubMed2001

Interaction of Bordetella pertussis with mast cells, modulation of cytokine secretion by pertussis toxin.

Together with macrophages and dendritic cells, mast cells have recently been shown to interact with certain pathogenic bacteria and present microbial antigens to the immune system. We show here that Bordetella pertussis can adhere to and be phagocytosed by mast cells. In addition, mast cells are able to process and present B. pertussis antigens to T lymphocytes. Furthermore, exposure of mast cells to B. pertussis induced the release of the proinflammatory cytokines tumour necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6). The release of IL-6 was strongly reduced by pertussis toxin expressed by B. pertussis. The production of IL-10, but not that of IL-4, by mast cells was also inhibited by pertussis toxin. Depletion of mast cells in vivo resulted in significant reduction of early TNF-alpha production in bronchoalveolar lavage (BAL) fluids of B. pertussis-infected mice. These data suggest that mast cells may play a role in the induction of immune responses against B. pertussis through the release of cytokines, especially TNF-alpha.

Animals↗
PubMed2006

Endothelial cell activation by mast cell mediators.

Mast cells are important cells of the immune system, and their secretory products regulate many vascular functions. Although considerable interest is focused on the role of mast cells and infectious agents in atherosclerosis, whether or not mast cell mediators act in concert with bacterial agents to regulate endothelial activation is not known. Here, we have described experimental techniques and presented related results to demonstrate how mast cell granule (MCG) mediators and bacterial products synergize endothelial cell inflammatory responses. The described methods outline: (1) the collection of rat peritoneal mast cells; (2) preparation of MCGs; (3) co-culture of human endothelial cells with mast cell granules; (4) determination of the regulation of endo- thelial cell inflammatory responses; (5) demonstration of the role of MCG protease and histamine in the regulation of endothelial cell function; (6) amplification of lipopolysaccharide-induced signal transduction pathways by mast cell granules; (7) elucidation of histamine-induced amplification of endothelial cell responses to Gram-negative and Gram-positive bacterial cell wall components; and (8) determination of the expression of Toll-like receptor 2 and 4. We hope the techniques described here can be used for designing experiments focusing on the regulatory role of mast cell mediators on cell functions.

Animals↗
PubMed1976

3H-Thymidine labeled mast cells in mice treated with 20-methylcholanthrene: proliferation of precursor cells, their transformation into mast cells and migration of the latter.

In an attempt to clarify the kinetics of increase of mast cells, autoradiographic studies were performed on the mice which received a painting of 20-methylcholanthrene on the skin. In the first experiment, mice received 20-methylcholanthrene painting on their back for two, four and eight weeks. A fourty-eight hours' cumulative labeling with 3H-thymidine was performed directly before sacrifice. No labeled mast cells were found in the painted skin, despite a marked increase of mast cells in number. In the second experiment, mice received 20-methylcholanthrene painting for thirty-one days. A twenty-four hours' cumulative labeling was performed three, five, seven, fourteen, twenty-one and thirty-one days before sacrifice. A high labeling index of mast cells, up to 61.29%, was obtained in each group. When the time lapse between the time of cumulative labeling and the sacrifice is long, the labeling index is higher in the subcutaneous tissue, and when the time lapse is short, the labeling index is higher in the subepidermal tissue. From these results it was concluded that; 1) An increase of mast cells is due predominantly to the proliferation of precursor cells and their transformation into mast cells. 2) The proliferation of precursor cells occurs mainly in the subepidermal layer of the skin. 3) After the transformation, mast cells may migrate into the deeper layer of the skin.

Administration, Topical↗
PubMed2002

Mast cell chymase regulates dermal mast cell number in mice.

Chymase inhibitor reduced the increase in the number of dermal mast cells in 2,4-dinitrofluorobenzene-induced dermatitis in a dose-dependent manner. Intradermal injection of human chymase to mouse ear significantly increased histamine content, the marker for mast cell number in the skin. These results suggest that chymase released by mast cells may participate in local mast cell accumulation in a positive feedback fashion. Immunohistochemical analysis revealed that the intradermal injection of chymase reduces expression of stem cell factor (SCF) on surface of the skin keratinocytes. In addition, incubation of human keratinocytes with chymase in vitro resulted in release of SCF into the culture medium. Since soluble SCF is thought to regulate mast cell number, the chymase-induced mast cell accumulation may occur via the ability of chymase to process membrane-bound SCF on the epidermal keratinocytes.

Animals↗
PubMed1998

Human bone marrow mast cells from indolent systemic mast cell disease constitutively express increased amounts of the CD63 protein on their surface.

The quantitative measurement of the expression of both cytoplasmic and surface CD63 antigen by human mast cells from both normal and pathological bone marrow samples was studied by use of flow cytometry. Our major goal was to analyze whether in vivo CD63 expression by human bone marrow mast cells could be useful to discriminate bone marrow mast cells from patients with mastocytosis from other conditions. For that purpose, a total of 65 subjects corresponding to 12 healthy volunteers, 25 B-cell chronic lymphoproliferative disorders, 5 reactive bone marrow samples, 4 myelodysplastic syndromes, and 19 mastocytosis were analyzed. The expression of both surface and cytoplasmic CD63 by human bone marrow mast cells is clearly demonstrated. Our results show that high amounts of CD63 are present in human bone marrow mast cells most of it corresponding to an intracellular localization. No significant differences in CD63 expression were observed as regards both total and cytoplasmic CD63, except for higher CD63 levels in adult patients with mastocytosis (P = 0.05). By contrast, the mean level of surface CD63 significantly varied between the different groups of individuals. Accordingly, patients with monoclonal gammopathies displayed a slight decrease (P = 0.1) in surface CD63 expression, whereas bone marrow mast cells from adults with indolent systemic mast cell disease showed significantly (P = 0.0005) higher levels of surface CD63 as compared to healthy controls.

Adult↗
PubMed2001

Endothelin-1 in smooth muscle cells and mast cells of mouse uterus after parturition.

To elucidate the physiological importance of endothelin-1 (ET-1) in mouse uterus, we investigated quantitative changes in ET-1 mRNA levels in the uterus during the estrous cycle, pregnancy and post-parturient period by use of the real-time PCR technique and we examined the cellular distribution of the ET-1 peptide by use of immunohistochemical techniques. Low and constant mRNA levels were observed in the uterus from cyclic or pregnant mice. However, a significant increase in mRNA levels was found immediately after parturition (day 0 postpartum) which then decreased gradually to a basal level at day 14 postpartum. Discernible immunopositivity was found in myometrial cells as well as in endometrial epithelial cells in the post-parturient uterus. Myometrial cells showed the strongest staining at day 0 postpartum, and some large cells in the myometrial layers, intensely positive for ET-1, were characterized as mast cells. These findings suggest the possibility that in mouse uterus ET-1 may play a role in recovery from the uterine changes caused by pregnancy and parturition.

Animals↗
PubMed1983

In vitro production of granular T cells and mast cells by use of different conditioned media. Ultrastructural and functional analysis.

Normal mouse spleen cells were cultured in different conditioned media (CM). Mixed lymphocyte culture supernatant (MLC SN) was shown to promote the proliferation of cytotoxic, Thy-1+, Lyt-1+, Lyt-2+, asialo-GM-1+, weakly adherent cells with numerous vacuoles and lysosome-like cytoplasmic granules. In contrast, the Con A SN induced the proliferation of non-cytotoxic, Thy-1-, Lyt-1-, Lyt-2-, asialo-GM-1-, non-adherent cells with numerous cytoplasmic granules. The ultrastructural morphology of these cells and the cytochemical characteristics of their granules enable us to identify them as mast cells. The different effects of both CM could be related to their T-cell growth factor (TCGF) content. When the amount of TCGF of these two CM was determined (by assaying growth-stimulating activity for T-cell colonies), it appeared that the MLC SN contained larger amounts of TCGF than the Con A SN used in these experiments.

Animals↗
PubMed1989

Novel structures CTLA-2 alpha and CTLA-2 beta expressed in mouse activated T cells and mast cells and homologous to cysteine proteinase proregions.

Differential screening of a subtracted cDNA library led to the detection of two distinct but homologous mouse cDNA, called CTLA-2 alpha and CTLA-2 beta. The corresponding transcripts have a tissue distribution restricted to T lymphocytes, where they are inducible upon activation, and to mast cells. The open-frame regions of both cDNA encode proteins homologous to cysteine proteinase precursors, remarkably, however, only to the proregion of these. The ctla-2 alpha and ctla-2 beta genes both map to the C1 band of mouse chromosome 13. Sequence comparisons suggest that the proregion of an ancestor proteinase gene evolved to the ctla-2 genes by successive duplications, first to autonomy, then to amplification. These results raise the question of the possible role of cysteine proteinase proregions, of cysteine proteinases themselves and of inhibitors thereof in activated T lymphocytes; from a different point of view, they also show that some protease proregions may have evolved as autonomous modules.

Amino Acid Sequence↗
PubMed2006

Mast cells enhance T cell activation: importance of mast cell costimulatory molecules and secreted TNF.

We recently reported that mast cells stimulated via FcepsilonRI aggregation can enhance T cell activation by a TNF-dependent mechanism. However, the molecular mechanisms responsible for such IgE-, Ag- (Ag-), and mast cell-dependent enhancement of T cell activation remain unknown. In this study we showed that mouse bone marrow-derived cultured mast cells express various costimulatory molecules, including members of the B7 family (ICOS ligand (ICOSL), PD-L1, and PD-L2) and the TNF/TNFR families (OX40 ligand (OX40L), CD153, Fas, 4-1BB, and glucocorticoid-induced TNFR). ICOSL, PD-L1, PD-L2, and OX40L also are expressed on APCs such as dendritic cells and can modulate T cell function. We found that IgE- and Ag-dependent mast cell enhancement of T cell activation required secreted TNF; that TNF can increase the surface expression of OX40, ICOS, PD-1, and other costimulatory molecules on CD3(+) T cells; and that a neutralizing Ab to OX40L, but not neutralizing Abs to ICOSL or PD-L1, significantly reduced IgE/Ag-dependent mast cell-mediated enhancement of T cell activation. These results indicate that the secretion of soluble TNF and direct cell-cell interactions between mast cell OX40L and T cell OX40 contribute to the ability of IgE- and Ag-stimulated mouse mast cells to enhance T cell activation.

Animals↗