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)

Allergic bronchopulmonary aspergillosis (ABPA) is a hypersensitivity lung disease caused by bronchial colonization with Aspergillus fumigatus that affects approximately 10% of patients with cystic fibrosis (CF). The diagnosis in CF patients is difficult because the cardinal symptoms of ABPA occur frequently in CF, ie, pulmonary infiltrates and wheezing, as well as the frequent colonization with A fumigatus that leads to humoral reactivity. If left untreated, ABPA leads to bronchiectasis and pulmonary fibrosis. The pathogenesis of ABPA seems to be a prolonged asthmatic late-phase reaction orchestrated by CD4+ Th2-like T cells in response to persistent pulmonary A fumigatus allergen exposure. Thus, polyclonal and A fumigatus-specific IgE antibodies (and IgA and IgG) and blood pulmonary eosinophilia are stimulated by Th2-derived cytokines such as IL-4 and IL-5. In addition, IL-4 would also promote pulmonary transendothelial migration of eosinophils, basophils, and lymphocytes via induction of cell adhesion molecules and their ligands. IgE mast cell interactions would also contribute to the bronchial reactivity and inflammation. Recent advances have begun to identify immunodominant A fumigatus allergens. Evaluation of the quantity of IgE antibodies (and IgA and IgG) and T-cell cytokine responses to specific A fumigatus allergens should aid in the diagnosis and immunopathogenesis of ABPA, especially in CF patients.
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PMID:Allergic bronchopulmonary mycosis complicating cystic fibrosis. 147 42

The presence of circulating IgG, IgA and IgM antibodies to native cartilage collagens in some patients with rheumatoid arthritis (RA) suggests that an autoimmune response to cartilage collagens may be involved in the pathogenesis of RA. However, the relevance of such antibodies to the pathological process remains unclear, and it is likely that many humoral and cellular derived factors combined to trigger events leading to the chronicity of the rheumatoid lesion. Since histological and biochemical studies have suggested the involvement of mast cells in the rheumatoid joint, we have studied the frequency of IgE antibodies directed against the cartilage collagens type II, IX and XI in patients with active rheumatoid disease. Of the 91 patients' sera tested, 32 had significant levels of IgE anti-cartilage collagen antibodies when compared with non-arthritic controls. Total serum IgE levels did not correlate with the presence of IgE anti-collagen antibodies, nor were any patients positive for IgE antibodies to fibronectin, a widely distributed extracellular matrix component. These results are consistent with an allergic type I hypersensitivity reaction to cartilage antigens in RA involving mast cell and basophil degranulation.
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PMID:Serum IgE anti-cartilage collagen antibodies in rheumatoid patients. 186 71

Five mouse strains, CBA/J, BALB/c, C3H/HeJ, A/J, and C57Bl/6J-bg-bg, all showed similar expulsion kinetics for Nippostrongylus brasiliensis (infective dose = 500 L3). Typically, parasite recovery was maximal on day 2 in the lungs and by day 4 in the small intestine. Few worms (less than 5% infective dose) were recovered on day 14 in all strains. These same mouse strains exhibited immune depression on day 5 of infection with mesenteric lymph node cells (MLN) showing reduced (10-30% normal) IgM, IgG, and IgA responses against heterologous antigen. The intestinal mast cell numbers and tissue histamine levels were examined in CBA/J mice. Mast cell numbers increased (normal = less than 1/villous crypt unit; VCU) from day 5 and peaked on day 12 (greater than 15/VCU). Intestinal histamine levels did not completely correlate with mast cell numbers with maximum concentrations (240 +/- 73 ng/g, 2-fold over normal) reached by day 8. Histamine concentrations in the intestine returned to normal levels by day 20.
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PMID:Characterization of Nippostrongylus brasiliensis infection in different strains of mice. 235 68

Our studies have clearly shown that neuropeptides have a profound effect on immunoglobulin synthesis both in vivo and in vitro. The effects varied according to the neuropeptide added or the tissue from which the lymphocytes were obtained. Substance P caused the most pronounced enhancement of both functions, especially in Peyer's patch cells, where it selectively increased IgA synthesis. Somatostatin was inhibitory, and the effect of vasoactive intestinal peptide varied according to the source of the cells. We have previously shown that neuropeptides also cause mast cell secretion and that only substance P was effective in this regard on intestinal mucosal mast cells. Therefore, we looked for microanatomic relationships between peptidergic nerves and immune effector cells. Mast cells appear to have structural associations with neuropeptides-containing nerves in the intestine. Nerve growth factor, known to promote the growth of sensory afferent and sympathetic nerves, has significant direct effects on mast cells. In vitro, this substance caused enhanced antigen mediated histamine release and, in vivo, extensive mast cell hyperplasia. Also, in humans, we were able to produce increased numbers of mast cell/basophil colonies from peripheral blood in the presence of nerve growth factor.
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PMID:Neuropeptides and immunity. 244 42

Plasma histamine levels and the histologic, electronmicroscopic, and immunofluorescent analysis of skin biopsy specimens were examined during the development of vibration-induced angioedema in two patients. The reactions to vibration in these patients were characterized by (1) clinical angioedema peaking 4 to 6 hours after challenge, (2) evidence of mast cell degranulation as indicated biochemically by an early and late increase in plasma histamine and histologically by exocytosis of mast cell granules, (3) a progressive infiltration of inflammatory cells, coinciding with the peak clinical reaction, and (4) an absence of the immunoreactants IgG, IgM, IgA, C3, and fibrinogen. The reactions in both patients were morphologically and biochemically similar to the cutaneous late-phase allergic reactions that occur after IgE-mediated, antigen-provoked mast cell degranulation. These studies suggest that vibratory angioedema is a manifestation of mast cell-induced cutaneous late-phase reactions.
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PMID:Delayed vibratory angioedema: insights into pathophysiologic mechanisms. 244 43

The recent identification of a T-cell-derived antigen-binding molecule (TABM), Trichinella spiralis factor (Tric-F), isolated from culture supernatants of lymphoid cells from mice infected with the intestinal helminth T. spiralis, has led to investigation of the ability of Tric-F to induce a T-cell-dependent feedback circuit that ultimately suppresses the production of other TABMs with similar (isotype-like) features. This form of regulation that has been identified in contact hypersensitivity and in delayed-type hypersensitivity (DTH) responses to tumor cells, was shown not to be antigen-specific but to be DTH-specific. Injection of mice with the TABM called picryl chloride factor (PCl-F) induced suppression of the production of DTH-initiating TABMs of other antigenic specificities. In this study, we report that intravenous injection of mice with Tric-F or PCl-F, 8 days before an oral infection with T. spiralis, induced suppressor cells that inhibited the T-cell-dependent influx into the gut of inflammatory cells, comprising mast cells and eosinophils. Similar results were obtained when the mice were skin sensitized with PCl 8 days prior to a T. spiralis infection, i.e. in a system where TABMs are known to be produced. The phenotype of these suppressor cells was Lyt-1-2+. This suppression preferentially affected the parasite-induced DTH-like response in the gut. In contrast, increased levels of IgA plasma cells in the gut, and worm expulsion were not affected by these treatments. In reciprocal experiments, intravenous injection of Tric-F, or PCl-F, or an oral infection with T. spiralis (that results in the production of TABMs) given 8 days before contact sensitizing mice with PCl, resulted in a suppression of elicitation of cutaneous DTH, as measured by ear swelling. In contrast, pretreatment with anti-dinitrophenyl IgE antibody did not interfere with intestinal inflammation to T. spiralis nor with DTH to PCl. Our results suggest that similar to cutaneous DTH, T. spiralis-specific T-cell factors are involved in the initiation and regulation of the DTH-like mast cell and eosinophil-rich intestinal inflammation that accompanies T. spiralis infections in the gut. Since both Tric-F and PCl-F induce suppression of cellular immune responses in vivo, independent of antigen specificity, it is concluded that Tric-F belongs to the same isotype of TABMs as PCl-F that therefore can be regulated by a non-antigen-specific, isotype-like, T-cell-dependent feedback mechanism.
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PMID:Antigen-specific T-cell factors induce isotype-like suppression of mast cell and eosinophil-rich T-cell-dependent inflammation in the intestine of mice infected with Trichinella spiralis. 258 51

Because of the tremendous impact that parasitic infections have on the health and productivity of humans and domestic animals, considerable research effort has been focused upon understanding the mechanisms of host-parasite coexistence, host resistance and immunopathology. Studies have employed a range of approaches including: kinetic analysis of parasite establishment, development, fecundity and survival in naive and previously-infected hosts; correlation between parasite survival and histopathologic responses at the site of infection; vaccination with attenuated parasites or their products; cellular and serum transfer of immunity to naive or immunocompromised hosts; pharmacologic manipulation of potential mediators of host defense using agonistic and antagonistic drugs. However, it is becoming increasingly clear that to understand the mechanisms associated with host resistance and parasite survival, one must define the characteristics of the local microenvironment at the host-parasite interface. One of the approaches by which such studies can be made involves the isolation and characterization of cells derived from the local infection site. This manuscript reviews some of these studies on local aspects of mucosal immune responses in parasitic infections. Examples that will be discussed include IgA antibody, intraepithelial leukocytes from the intestine, intestinal mast cell populations, macrophages derived from bronchoalveolar lavage, and local immunoregulatory responses during respiratory and intestinal parasitic infection. These studies have established unequivocally that local responses to mucosal parasitic infection can only be appropriately investigated using cells derived from the specific microenvironment. This conclusion should encourage others to further study these local responses and to be innovative in investigating unexplored aspects of the host-parasite interface.
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PMID:Unique characteristics of local responses in host resistance to mucosal parasitic infections. 351 14

Light- and electronmicroscopic observations as well as immunohistochemical studies were made on nasal polyps from 15 patients. The patients included 2 cases of aspirin intolerance (AA), 6 cases of allergic rhinitis (NA) and 7 cases of chronic rhinitis (CS) with negative skin tests against major inhalant allergens. Nasal polyps commonly contained many inflammatory cells such as neutrophils (PMN), eosinophils, plasma cells, mast cells, lymphocytes and macrophages. Two morphological features were conspicuous in our study: 1) PMN migration and attachment to the basal lamina, 2) accelerated degranulation of mast cells. Mean values of degranulated granules were 0.532473/micron2 in AA, 0.492615/micron2 in NA and 0.253591/micron2 in CS. These results indicate that mast cell degranulation in CS is much less than that in AA and NA. Immunohistochemical investigations revealed very few IgE-positive cells in both AA and NA, and none in CS. On the other hand IgG and IgA were frequently observed in all cases of nasal polyps. The present study suggests that mast cell degranulation plays an important role in the formation of nasal polyps, but it may not only be an IgE-dependent mechanism. To elucidate other possibilities, more extensive immunological studies will be required.
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PMID:Mast cell degranulation in nasal polyps. 352 8

This work is concerned with new morphologic data pointing to an immune component in the pathogenesis of pseudomembranous colitis. The focal distribution of the pseudomembranes suggests selective damage induced by Clostridium difficile toxins. The sites of attachment to the mucosa correspond anatomically to the intestinal structures specialized for immune information and response. Furthermore, viable IgA production supports the view that toxins are carried to lymphoid aggregates where plasma cell proliferation takes place. A sharp increase in the mast cell population of the colon is also reported. Mast cells, whose role in the pathogenesis of intestinal diseases is still obscure, are diffusely distributed, irrespective of the focal lesions of pseudomembranous colitis.
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PMID:Pathogenesis of pseudomembranous colitis. 388 23

Relations between the appearance of various components of the immune response were analyzed in two groups of rats sensitized by aerosol and subcutaneous injections in the neck region, respectively. The relations were expressed by Spearman rank correlation coefficient and studied by cluster analysis. In the aerosol-sensitized animals, there was a close association between IgA and IgG antibody levels in bronchial fluid and these in turn were related to IgG levels in serum and more loosely to IgE levels in bronchial fluid. There was an apparent association between IgE antibody formation and mast cell maturation in cultures of regional lymph node cells and the appearance of mucous cells in the lungs. These variables seemed associated with spontaneous cell proliferation in vitro and the numbers of mast cells in the lungs. This indicates that local stimulation with antigen induces local immune responses and immune-mediated migration of cells. In subcutaneously sensitized animals, formation of IgG antibodies in vitro seemed related to the stimulated proliferation of regional lymph node cells. The levels of IgG and IgE antibodies in bronchial fluid and in serum also appeared to be related. Unlike the findings in aerosol-sensitized animals there was no apparent relation between the differentiation of mast cells and mucous cells. This was possibly due to lack of immune-mediated antigen-induced cell migration. The different immune response patterns in aerosol and subcutaneously sensitized rats should be considered when studies are designed aiming to explore the pathogenesis of allergic inflammatory diseases. The findings also indicate that the various parameters of immunity are more closely related in aerosol than in subcutaneously immunized animals.
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PMID:Relation between components of the immune response in rats sensitized by aerosol and subcutaneous injections. 396 32


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