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 pathogenesis of parainfluenza 1 (Sendai) virus infection was compared among 25-day-old BN, F344, and LEW rats to identify a sensitive as well as a resistant inbred rat strain to Sendai virus-induced lung injury during early life. At 7 days after inoculation, BN rats had 65-fold higher (P less than .001) pulmonary viral titers and threefold higher (P less than .002) numbers of neutrophils in bronchoalveolar lavage fluid than did F344 rats. At 14 days after inoculation, when most virus-induced inflammation had been resolved, BN rats had a threefold greater (P less than .01) incidence of bronchioles with aggregates of lymphocytes and macrophages than did F344 rats. Control BN rats had higher numbers of bronchiolar eosinophils than did F344 or LEW rats. Although viral inoculation resulted in increased numbers of bronchiolar mast cells in all three strains at 14 days, bronchiolar mast cell density was greater (P less than .005) in virus-inoculated BN and LEW rats than in F344 rats. We conclude that BN rats are high responders and F344 rats are low responders to Sendai virus-induced bronchiolitis, pneumonia, and airway mastocytosis. These strain differences may be useful in elucidating important pathogenetic mechanisms in virus-induced airway injury and mastocytosis.
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PMID:Brown Norway rats are high responders to bronchiolitis, pneumonia, and bronchiolar mastocytosis induced by parainfluenza virus. 166 31

Previous studies showed that lung and skin mast cells do not contain eosinophil granule major basic protein (MBP). However, MBP has been localized by immunofluorescence to mast cells from a recently established human mast cell line. Analysis of MBP in human mast cell-1 cell lysates by radioimmunoassay showed immunochemical similarity to eosinophil MBP as judged by comparison of dose-response regression lines. Based on these findings and other new information about mast cell heterogeneity, we tested whether mast cells contain MBP. Mast cells were preserved in Carnoy's fixative and were identified by staining with rhodamine-conjugated avidin or for chloroacetate esterase or aminocaproate esterase activity. MBP was localized by immunofluorescence to mast cells in 6 of 7 nasal polyps, 4 of 4 ileal tissue specimens, and 12 of 14 cutaneous mastocytosis specimens. Furthermore, by immunoelectron microscopy MBP was localized to mast cell granules in cutaneous mastocytosis lesions. In contrast, normal skin mast cells preserved in Carnoy's fixative did not contain MBP. After injection of MBP into normal skin and fixation in Carnoy's fluid, mast cells became MBP-positive within 3 minutes, suggesting that endocytosis of MBP by mast cells had occurred. These results suggest that human mast cells in several tissues may sequester toxic eosinophil proteins by endocytosis.
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PMID:Sequestration of eosinophil major basic protein in human mast cells. 168 35

Nerve growth factor (NGF) is a neurotropic polypeptide which has broad biological activity other than support of growth and survival of sympathetic, sensory and central neurons. NGF promotes rat mast cell hyperplasia in vivo and human granulopoiesis in vitro, selectively augmenting basophil/mast cell differentiation in the presence of T cells or conditioned medium derived from a human T cell line (Mo-CM), a source of granulocyte-macrophage colony-stimulating factor (GM-CSF). NGF also synergizes with GM-CSF to promote human basophil/mast cell differentiation in both methylcellulose and suspension cultures of myeloid progenitors. In the current studies, we examined the interactions of NGF and several cytokines considered to be involved in human basophil/mast cell and eosinophil growth and differentiation, including interleukin (IL)-3, IL-4, IL-5, GM-CSF and granulocyte colony-stimulating factor (G-CSF). NGF synergistically enhanced IL-5 induced dose-dependent increases in histamine content and basophilic cell differentiation of myeloid leukemic HL-60 cells, but was only additive to similar effects of IL-3. In contrast, IL-4 and G-CSF did not promote basophilic differentiation of HL-60 cells in the presence or absence of NGF. Various combinations of GM-CSF, G-CSF, IL-3, IL-4 and IL-5 could not reproduce the synergy observed between NGF and either IL-5 or GM-CSF. NGF appears to represent a class of lineage-specific co-factors, in this case being involved in GM-CSF- or IL-5-induced basophilic lineage differentiation, thus contributing to tissue inflammation or repair.
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PMID:Interactions of hemopoietic cytokines on differentiation of HL-60 cells. Nerve growth factor is a basophilic lineage-specific co-factor. 169 Jan 80

The onset of mastocytosis occurs between birth and 2 years of age in approximately 55% of all cases; an additional 10% develop the disease before the age of 15 years. Mastocytosis in these age groups differs in many respects from mastocytosis that has its onset in adulthood. The typical presentation of pediatric-onset mastocytosis consists of cutaneous manifestations: either a solitary mastocytoma, urticaria pigmentosa, or, less commonly, diffuse cutaneous mastocytosis. Particularly in infants, bullous eruptions may occur. Mastocytosis in infants and children may involve internal organs, including the bone marrow and the gastrointestinal tract, although such manifestations appear to be less common in children than in adults. Plasma histamine levels may be elevated in pediatric-onset mastocytosis. Treatment usually involves the use of H1 and H2 antihistamines to control itching and to control the hypersecretion of gastric acid that may occur. The prognosis for children with mast cell disease is variable; approximately half of the children with urticaria pigmentosa may experience resolution of lesions and symptoms by adolescence.
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PMID:Pediatric mastocytosis. 170 49

A human cell strain (designated HBM-M) that was derived from the bone marrow of a child with diffuse cutaneous mastocytosis was previously found to possess features that suggested it belonged in the mast cell/monocyte lineage. HBM-M cells synthesized approximately 150-Kd Pronase-resistant proteoglycans that were recognized by an antihuman secretory granule proteoglycan peptide core antibody. These cells also contained in relatively high abundance the same sized mRNA transcript that encodes the peptide core of proteoglycans that are normally localized to secretory granules of hematopoietic cells. However, unlike most other hematopoietic cells, HBM-M cells continuously released their newly synthesized 35S-labeled proteoglycans rather than retaining them in an intracellular storage compartment. Chondroitinase ABC, nitrous acid, and heparinase degraded approximately 76%, 17%, and 7%, respectively, of the HBM-M cell-derived 35S-labeled proteoglycans. As assessed by high performance liquid chromatography, 91% of the unsaturated 35S-labeled disaccharides generated by treatment with chondroitinase ABC were delta Di-4S. The remaining chondroitin sulfate 35S-labeled disaccharides appeared to be primarily a complex mixture of disulfated disaccharides. The 35S-labeled glycosaminoglycans that were not degraded by chondroitinase ABC migrated in two-dimensional cellulose acetate electrophoresis as if they were heparan sulfate or under-sulfated heparin. Thus, although the HBM-M cell-derived proteoglycans had some of the features of proteoglycans produced by normal human mast cells, the heparin-like and chondroitin sulfate glycosaminoglycans bound to the HBM-M cell proteoglycans were considerably less sulfated. Because the only human cell types that have so far been shown to synthesize proteoglycans that have heparin-like glycosaminoglycans bound to a protease-resistant peptide core are mast cells and basophilic leukocytes from patients with myelogenous leukemia, it is possible that the HBM-M cell is a mast cell progenitor cell.
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PMID:Continuous release of secretory granule proteoglycans from a cell strain derived from the bone marrow of a patient with diffuse cutaneous mastocytosis. 172 5

A 48 year old male patient presented with maculopapular rash, pruritus, peptic ulcer disease and attacks of headache and vertigo. Rubbing of the cutaneous lesions led to urticarial whealing which is indicative of abnormal mast cell proliferation in the cutis. Histologic evidence of abnormal mast cell proliferation in biopsy specimens of skin and bone marrow led to the diagnosis of systemic mastocytosis. Treatment with H1 and H2 receptor antagonists was started.
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PMID:[Maculopapular rash, pruritus, upper abdominal pain, attacks of dizziness]. 174 78

A myelodysplastic syndrome (MDS), type 5 (RAEB-t), and systemic mastocytosis affecting the spleen, the splenic lymph nodes, the bone marrow and the liver were diagnosed in a 38-year-old woman. The clinical course was complicated by splenic vein thromboses and iliac artery embolism. The thrombotic episodes might be secondary to mast cell mediator release. A complete remission of the MDS was obtained by allogeneic bone marrow transplantation, but the mastocytosis persisted. Thus, the possibility that the mast cell originates from a common myeloid precursor cell may be questioned.
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PMID:Persistence of systemic mastocytosis after allogeneic bone marrow transplantation in spite of complete remission of the associated myelodysplastic syndrome. 176 77

Systemic mastocytosis is a rare condition in which mast cells infiltrate various organs, including the skeleton. Because the mast cell secretes various bioactive substances that may induce bone resorption, this condition may cause generalized osteoporosis. We describe a case of a 28-year-old woman who presented with a painful thoracolumbar kyphosis due to generalized osteopenia and multiple pathological compression fractures and was found to have mastocytosis. She underwent operative stabilization of her kyphotic deformity with anterior interbody fusion and posterior Cotrel-Dubousset (CD) instrumentation and fusion. We conclude that mastocytosis should be suspected in an atypical case of so-called idiopathic osteoporosis.
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PMID:Systemic mastocytosis presenting with severe spinal osteopenia and multiple compression fractures. 180 68

Parasitological and immunological responses of genetically resistant and random-bred lambs to primary and secondary infection with H. contortus were studied. Resistant lambs had higher faecal egg counts and total worm burdens than the random-bred lambs following the primary infection. As there were no significant differences in serum and antibody levels, mucosal mast cells, circulating and tissue eosinophils between the two groups, it is inferred that what ever the underlying mechanism it was an innate characteristic. In contrast to primary infection, resistant lambs had significantly lower faecal egg counts and worm burdens than the random-bred lambs on secondary infection. Resistant lambs also exhibited significantly higher antibody levels, mucosal mast cell hyperplasia and mucosal eosinophilia in response to a challenge infection than the random-bred lambs. Furthermore, levels of mast cell hyperplasia and anti-Haemonchus antibodies correlated positively with the resistance status of the host. Taken together these results suggest that the genetic resistance of sheep to H. contortus results from the expression of an acquired immune response, and that anti-parasite antibodies and mast cell-derived mediators may play an important role in genetically determined resistance of sheep to haemonchosis.
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PMID:Genetic control of acquired resistance to haemonchosis in Merino lambs. 181 Dec 13

Intestinal mucosal mast cells (IMMCs) are closely apposed to nerves, which is consistent with other evidence suggesting that mast cells are innervated. Recent studies have indicated that coordinated changes in mast cell and nerve densities occur in the gut mucosa, during progressive fibrosis, but there is a lack of experimental evidence to support remodeling of intestinal nerve fibers as part of a disease process. Infection of rats with the nematode Nippostrongylus brasiliensis (Nb) results in an initial loss of stainable IMMCs, during an acute inflammatory phase, with subsequent mast cell hyperplasia. Accordingly, we employed the Nb model to look for structural neuroplasticity of intestinal mucosal nerves during inflammation. Immunocytochemical labeling of neurofilament subunits was very low in the jejunal mucosa of all animals, whereas neuron-specific enolase (NSE)-immunoreactive nerves were relatively abundant in control animals. The number of NSE-immunoreactive profiles increased approximately 2.5-fold by day 10 (d10) postinfection (p less than 0.01) and returned to near control values by d14. Immunoreactivity for B-50/GAP-43 was more extensive, labeling more than four times the number of nerves per villus, compared with NSE (p less than 0.0001). B-50 immunoreactivity decreased minimally (ca. 20%) by d7 postinfection, and then increased through control values between d10 and d21, to 30% greater than controls at d49 (p less than 0.05). Subclassification of the B-50-immunoreactive nerves according to cross-sectional area revealed a greater than twofold increase in the proportions of large fibers at d7 and d10. Subsequently, the proportions of small nerves were increased compared with controls. The fiber size changes were found to correlate with mast cell densities (r = -0.72 for large and r = 0.76 for small nerves). At d10, dilated B-50- and NSE-immunoreactive nerves predominated, and extraneuronal NSE was noted. Electron microscopy revealed that this was due to axonal dilation and degeneration. These data provide evidence for plasticity of intestinal mucosal nerve fibers during inflammation. This includes early degenerative and later regenerative phases that appear to correlate with mast cell densities. The phenotype of mucosal nerves in control animals suggests ongoing modeling of these fibers.
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PMID:Remodeling of B-50 (GAP-43)- and NSE-immunoreactive mucosal nerves in the intestines of rats infected with Nippostrongylus brasiliensis. 183 18


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