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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mice exposed to primary infections with the parasite intestinal nematode Nematospiroides dubius failed to show the mucosal mast cell (MMC) response which is characteristic of infections with other species of intestinal nematode and which was readily induced in these mice by infections with Nippostrongylus brasiliensis or Trichinella spiralis. The failure to generate a mucosal mastocytosis was independent of host strain or sex. When infections with N. dubius were established before, or concurrently with, T. spiralis or N. brasiliensis, the MMC response elicited by these species was delayed and/or depressed as was expulsion of the worms themselves. Infection with N. dubius given when a MMC response was already established, by exposure to T. spiralis, had no effect on MMC numbers. The possibility that the effects of N. dubius upon MMC responses reflect a lack of mastocytopoietic potential, rather than an active interference, was excluded by showing that SJL mice, which expel primary infections with N. dubius and express strong immunity to reinfection, developed marked mastocytosis during secondary infections. The depression of MMC responses by N. dubius is discussed in relation to the known immunosuppressive properties of this parasite and in relation to the T cell mediated control of MMC development.
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PMID:Suppression of mucosal mastocytosis by infection with the intestinal nematode Nematospiroides dubius. 357 74

To test the hypothesis that viral respiratory infections cause symptoms by activating mucosal mast cells to release mediators active on vasculature and mucosal glands, the presence of histamine in nasal secretions was assessed during natural colds and rhinovirus infections. Secretions were collected either with saline washes of the nasal cavity or by forcibly blowing into a beaker, and histamine was assayed spectrofluorometrically. In blown secretions from uninfected subjects, large variations were seen between individuals (ranging from 3 +/- 2 to 59 +/- 32 ng/ml), and equally large variations were seen from day to day in given subjects. Infection with rhinovirus and with influenza A did not change these concentrations significantly. In general, both with blown nasal secretions and with nasal washes, histamine concentrations tended to be lower during infection. Concentration of another preformed mast cell mediator, TAME-esterase, also was not elevated during infection. Thus, these data do not support an hypothesis that mast cell activation occurs during rhinovirus infections.
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PMID:Mediators of immediate hypersensitivity in nasal secretions during natural colds and rhinovirus infection. 609 51

Infection with the intestinal parasite Nippostrongylus brasiliensis stimulates an accumulation of mucosal mast cells (MMC) in the villi of the small intestine of normal but not athymic or W/Wv anemic mice. W/Wv mice are congenitally deficient in both MMC and skin and connective tissue mast cells (CTMC). Athymic mice have normal or elevated numbers of CTMC but are severely deficient in MMC. CTMC derive from the bone marrow. To determine the origin of MMC, athymic and W/Wv mice were given various hematopoietic or lymphoid tissues from normal littermate or beige mice and the MMC response to N. brasiliensis infection was evaluated. The MMC defect in athymic mice was repaired by grafts of thymus cells, thymus gland, or spleen cells, but not by bone marrow cells or anti-Thy 1-treated bone marrow or spleen cells. The MMC and CTMC defects of W/Wv mice were repaired by grafts of bone marrow, spleen cells, or anti-Thy 1-treated bone marrow or spleen cells. Neither the MMC nor the CTMC defect in W/Wv mice was repaired by grafts of thymus cells or thymus glands. These results indicate the following, MMC, like CTMC, derive from the bone marrow and not from the thymus. MMC require a thymic influence for development. Athymic mice possess bone marrow precursors for both MMC and CTMC but lack a thymus-dependent component necessary for MMC development. W/Wv mice lack both MMC and CTMC mast cell precursors but possess the thymus-dependent component required for MMC development.
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PMID:Bone marrow origin of mucosal mast cells. 636 92

Infection of guinea pigs with the parasitic nematode Trichostrongylus colubriformis was followed by a three- to fourfold increase in the number of mast cells in the small intestine mucosa. Mitotic figures were observed in many mast cells during the period numbers were increasing. Many mast cells developed cytoplasmic granules which, unlike pre-infection mast cell granules, contained crystalline structures.
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PMID:Intestinal mast cell changes in guinea pigs infected with the nematode Trichostrongylus colubriformis. 671 63

The connective tissue of rats, and several other species of mammals, contains two distinct types of mast cells that differ in morphology, histochemical staining properties and location1. One type, frequently called the normal connective tissue mast cell, can be obtained in nearly homogeneous preparation from a mixed cell population in the peritoneal cavity and forms the basis of our knowledge of mast cells. The other type is referred to as the mucosal mast cell because in normal rats it has been observed only in mucosal tissue. Infection with helminth parasites induces an exteNsive accumulation of mast cells and eosinophils in the tissues, and parasites of mucous surfaces, in particular, stimulate a rapid hyperplasia of mucosal mast cells. However, the origin of mucosal mast cells, and their relationship to the connective tissue mast cells is uncertain. We now slow that lymphocytes of helminth-infected rats, on in vitro stimulation with specific antigen, release factors causing pronounced mucosal mastocytosis in normal rat bone marrow cultures.
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PMID:Generation of mucosal mast cells is stimulated in vitro by factors derived from T cells of helminth-infected rats. 698 22

Infection by helminthic parasites can cause the polyclonal stimulation of IgE synthesis, possibly via an enhanced production of interleukin-4 (IL-4), and this has been suggested to influence the allergic reactivity of tropical populations where these parasites are endemic. We evaluated a group of urban slum children in Caracas, Venezuela, with a high prevalence of helminthic infection (70.8%), to establish the relationship between the elevated IgE levels (3696 IU/ml) induced by these parasites and various aspects of the allergic response. Although the absolute levels of IL-4 detected in the sera of these children were low (0.65 +/- 0.20 ng/ml), a strong positive correlation (r = 0.78) was found between these and serum IgE. The cutaneous immediate hypersensitivity reactivity to extracts of common environmental allergens was relatively low (17.5% to house dust), although that to Ascaris extract was moderately high (49.4%). Significant inverse correlations were found between total IgE levels and the different skin test reaction diameters, including Ascaris. The positivity of Prausnitz-Kustner passive transfer tests was low in this group (34%), with a strong inverse correlation (r = -0.75) being found between this and total IgE levels. Significant inverse correlations were also found between total IgE levels and specific IgE antibody to environmental allergens, and to Ascaris antigen. We suggest that the polyclonal production of IgE stimulated by helminthic infection can suppress the allergic response to environmental and parasite allergens via both mast cell saturation and inhibition of specific IgE production.
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PMID:Modulation of the allergic reactivity of slum children by helminthic infection. 836 73

Infection of airway epithelial cells with respiratory syncytial virus (RSV) results in the production of a restricted number of cytokines, which may modulate the inflammatory response to infection. To get a better understanding of epithelial cell-mediated inflammatory processes in RSV disease, the aim of the present study was to identify the production of mononuclear cell/eosinophil/mast cell inflammatory chemokines [monocyte chemotactic protein (MCP)-1, MCP-3, macrophage inflammatory protein-1beta, and RANTES] during productive RSV infection in airway epithelial cells. Normal human primary bronchial epithelial cell cultures, nasal epithelial cell explants, and the BEAS-2B airway epithelial cell line were inoculated with RSV, and chemokine induction was assessed during the phase of logarithmic increase in infectious virus production. Only RANTES was found to increase in epithelial cell cultures in an infection-dependent manner. Furthermore, RANTES was released only by RSV-producing cells. To determine whether RANTES was induced by RSV infection in vivo, RANTES was measured in nasal lavage fluids (NLF) from children with RSV-positive and RSV-negative upper respiratory infection and children when they were well. RANTES was increased significantly during RSV infection (128 +/- 38 pg/ml NFL) compared with non-RSV infection (42 +/- 12 pg/ml NFL) and with asymptomatic baseline (13 +/- 4 ng/ml NFL) in the same children. Because RANTES is an effective eosinophil and memory T cell chemoattractant and activator and because eosinophil-dominated inflammation is a hallmark of asthmatic airways, RANTES may play a role in the pathogenesis of RSV-induced exacerbations of airway reactivity and wheezing.
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PMID:RSV infection of human airway epithelial cells causes production of the beta-chemokine RANTES. 912 9

Long-Evans Cinnamon (LEC) rats have maturational arrest of CD4+8- T cells from CD4+8+ cells in the thymus. Despite this, CD4+8- T cells are always present in peripheral lymphoid organs of LEC rats, suggesting that these CD4+8- T cells are generated by an uncommon pathway. We investigated the role of LEC rat peripheral CD4+8- T cells in Th2-associated responses to infection with the nematode Nippostrongylus brasiliensis. After infection, the numbers of CD4+8- TCR alpha beta + T cells significantly increased in mesenteric lymph nodes (MLN) and the spleen, while those in the thymus were still negligible. Infection also induced significant up-regulation of IL-4 gene expression in LEC rat MLN cells. Total serum IgE levels in LEC rats were markedly increased two weeks after infection. Mucosal mast cell responses in the gut and lungs of LEC rats were induced as prominently as in control Long-Evans Agouti (LEA) rats. Faecal egg count data indicated that LEC rats rejected nematodes faster than LEA rats. These results suggested that Th2-associated responses can be induced by nematode infection in LEC rats probably through the extrathymic recruitment and proliferation of CD4+8- TCR alpha beta + T cells.
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PMID:Nematode infection induces Th2 cell-associated immune responses in LEC mutant rats with helper T cell immunodeficiency. 937 14

Giardiasis has been associated with an increase in allergic disease following infection suggesting an alteration in mucosal immune function. Jejunal in vivo and in vitro macromolecular transport, epithelial permeability, and mucosal and connective tissue mast cell counts were examined in Mongolian gerbils (35-45 g) orogastrically inoculated (I) with a pathogenic strain of Giardia lamblia and compared to age- and weight-matched, sham-treated controls (C) 6 and 21 days postinoculation. Macromolecular uptake was significantly increased in infected tissue at 6 days both in vivo (I 134 +/- 19 vs. C 74 +/- 17 ng/hr; n = 8; P < 0.05) and in vitro (I 125 +/- 17 vs. C 67 +/- 8 ng/hr/cm; n = 12; P < 0.05). Macromolecular uptake did not differ between groups at 21 days. Infection had no effect on mucosal permeability of [51Cr]EDTA. Mucosal mast cell counts did not differ at 6 days but were significantly elevated in infected tissue at 21 days (I 33.3 +/- 6.8 vs. C 2.7 +/- 0.4 per high magnification field; n = 5; P < 0.01) as were connective tissue mast cell counts (I 1.7 +/- 0.2 vs. C 1.0 +/- 0.1 per high magnification field; n = 13; P < 0.005). The findings indicate that during the peak phase of giardiasis, jejunal active antigen uptake is increased leading to a delayed recruitment of mucosal and connective tissue mast cells. These changes may play a role in the increased incidence of hypersensitivity reactions associated with Giardia infection.
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PMID:Mast cell hyperplasia and increased macromolecular uptake in an animal model of giardiasis. 937 97

We report here the first demonstration of dengue virus infection and vasoactive cytokine response of a cell of the mast cell/basophil lineage. Infection of KU812 cells was dependent on dengue-specific antibody and gave rise to infectious virions. This antibody-enhanced dengue virus infection triggered a four- to fivefold increase in the release of interleukin-1beta (IL-1beta) and a modest increase for IL-6 but not for an alternate cytokine, granulocyte-macrophage colony-stimulating factor. The results suggest a potential role for mast cells/basophils in the pathogenesis of dengue virus-induced disease.
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PMID:Release of vasoactive cytokines by antibody-enhanced dengue virus infection of a human mast cell/basophil line. 1088 55


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