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

Urticaria and angioedema evoke a completely different differential diagnosis from angioedema without an associated urticarial syndrome. This review of the literature is to give the reader a global insight into the spectrum of urticaria and angioedema, focusing on differential diagnosis and pathogenic mechanisms. It will define the role of the mast cell, explore a possible autoimmune basis for urticaria, and examine the purported role of food allergy in chronic urticaria. Last, the work-up and treatment will be discussed. Urticaria and angioedema are frustrating problems for both physicians and their patients; however, the problem can best be approached by considering urticaria as a symptom rather than a specific disease. The physical examination and medical history remain the two most important pieces of information.
Allergy Asthma Proc
PMID:Urticaria and angioedema. 1247 45

Adverse reactions to radiocontrast media (RCM) occur unexpectedly and may be life-threatening. This article describes an anaphylactoid reaction (AR) in one patient. The term AR refers to a syndrome clinically similar to anaphylaxis, but these reactions are independent of immunoglobulin E antibody-mediated mast cell or basophil degranulation. This article briefly reviews the literature regarding RCMs and types of reactions to RCM. The risk factors for AR to RCM infusions will be discussed along with current concepts of the pathogenesis of RCM-induced ARs. This article also describes the therapeutic management of patients who have had a previous adverse reaction to RCM and provides an approach to patients who have breakthrough reactions despite adequate premedication, but require additional radiographic studies.
Allergy Asthma Proc
PMID:Reactions to radiocontrast media. 1247 46

Exercise-induced anaphylaxis has been recognized with increasing frequency since its original description in 1980. Recent studies suggest food-induced reactions may occur frequently in this syndrome, which is a mast cell-dependent phenomenon. In this article, the clinical manifestations of exercise-induced anaphylaxis are reviewed, and food-related factors contributing to the disorder are considered.
Curr Allergy Asthma Rep 2003 Jan
PMID:Exercise-induced Anaphylaxis. 1254 88

Asthma results from an intrapulmonary allergen-driven Th2 response and is characterized by intermittent airway obstruction, airway hyperreactivity, and airway inflammation. An inverse association between allergic asthma and microbial infections has been observed. Microbial infections could prevent allergic responses by inducing the secretion of the type 1 cytokines, IL-12 and IFN-gamma. In this study, we examined whether administration of bacterial LPS, a prototypic bacterial product that activates innate immune cells via the Toll-like receptor 4 (TLR4) could suppress early and late allergic responses in a murine model of asthma. We report that LPS administration suppresses the IgE-mediated and mast cell-dependent passive cutaneous anaphylaxis, pulmonary inflammation, airway eosinophilia, mucus production, and airway hyperactivity. The suppression of asthma-like responses was not due to Th1 shift as it persisted in IL-12(-/-) or IFN-gamma(-/-) mice. However, the suppressive effect of LPS was not observed in TLR4- or NO synthase 2-deficient mice. Our findings demonstrate, for the first time, that LPS suppresses Th2 responses in vivo via the TLR4-dependent pathway that triggers NO synthase 2 activity.
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PMID:Bacterial lipopolysaccharide signaling through Toll-like receptor 4 suppresses asthma-like responses via nitric oxide synthase 2 activity. 1284 73

Asthma is currently defined as a chronic inflammatory disorder of the airways. The exact relationship between this inflammatory process and altered airway behavior in asthma remains to be fully established. More specifically, the question remains as to the exact causal relationship between airway inflammation and bronchial hyperresponsiveness (BHR), which constitutes the predominant lung function abnormality in asthma. The two main determinants of BHR are the hypersensitivity and the hyperreactivity of the airways. Hypersensitivity is reflected in a leftward shift of the dose response curve to the bronchoconstrictor effect of agonists such as histamine. More important from a clinical perspective is the hyperreactivity of the airways, which is characterized by excessive airway narrowing. The airway wall consists of three compartments, namely the inner airway wall area between the airway lumen and the smooth muscle layer, the airway smooth muscle layer and the outer airway wall area between the smooth muscle layer and the lung parenchyma. Mathematical models have calculated that changes within each of these compartments can contribute to airway hyperreactivity. Morphometric analysis of asthmatic airways confirm thickening of each of these three airway wall compartments. The contribution of airway inflammation to the thickening of each of these compartments and their relative functional impact on BHR remains to be further elucidated. Asthmatic airways display signs both of the acute and the chronic phase of an inflammatory reaction. The acute allergic inflammation is characterized by the presence of increased amounts of inflammatory cells including eosinophils, mast cells, macrophages, dendritic cells and T helper 2 (Th2) lymphocytes, and is regulated by a complex network of mutually interacting cytokines. The Th2 lymphocyte plays a crucial role within this network. Based, amongst other observations, on in vivo animal models, the hypothesis can be formulated that through the release of a range of cytokines, Th2 cells affect directly airway responsiveness. It would appear that neither crosslinking of IgE and subsequent mast cell degranulation nor eosinophil influx into the airways play a crucial role in this process. Asthmatic airways also display signs of a chronic inflammatory process, that results in more structural alterations, the so-called airway remodeling. This includes increased deposition of collagen and fibronectin, in addition to airway smooth muscle hypertrophy and hyperplasia. In vivo animal models indicate that these structural alterations have a more profound impact on BHR than the acute inflammation. These models also illustrate that depending on the exact extent and location of structural changes throughout the various airway wall compartments, remodeling can enhance but also protect against excessive airway narrowing, despite the presence of acute inflammation. These results illustrate the necessity to take into account the full extent of histological alterations throughout the airway wall, when evaluating the effect of individual cells and cytokines involved in the acute and chronic inflammatory response in asthma.
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PMID:[The relation between morphologic and functional airway changes in bronchial asthma]. 1453 40

Asthma is a chronic inflammatory disease of the airways. Mast cell-derived cytokines may mediate both airway inflammation and remodeling. It has also been shown that fibroblasts can be the source of proinflammatory cytokines. In the human airways, mast cell-fibroblast interactions may have pivotal effects on modulating inflammation. To study this further, we cocultured normal human lung fibroblasts (NHLF) with a human mast cell line (HMC-1) and assayed for production of interleukin (IL)-6, an important proinflammatory cytokine. When cultured together, NHLF/HMC-1 contact induced IL-6 secretion. Separation of HMC-1 and NHLF cells by a porous membrane inhibited this induction. HMC-1-derived cellular membranes caused an increase in IL-6 production in NHLF. Activation of p38 MAPK was also seen in cocultures by Western blot, whereas IL-6 production in cocultures was significantly inhibited by the p38 inhibitor SB203580. IL-6 production in cocultures was minimally inhibited by a chemical inhibitor of nuclear factor-kappaB (Bay11), indicating that nuclear factor-kappaB may have a minimal role in signaling IL-6 production in mast cell/fibroblasts cocultures. Blockade of inter-cellular adhesion molecule-1, tumor necrosis factor-RI, and surface IL-1beta with neutralizing antibodies failed to significantly decrease IL-6 production in our coculture, indicating that other receptor-ligand associations may be responsible for this activation. These novel studies reveal the importance of cell-cell interactions in the complex milieu of airway inflammation.
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PMID:Human lung fibroblasts express interleukin-6 in response to signaling after mast cell contact. 1456 41

Mast cells are involved in allergic inflammation and some rare disorders such as systemic mastocytosis and mast cell leukemia. Certain naturally occurring flavonoids have been shown to inhibit mast cell activation and promote maturation of secretory granules. Here, we report that the isoflavone genistein inhibited the growth of human leukemic mast cells (HMC-1) by 68.8, 51.6, and 30.2% at 10(-4), 10(-5), and 10(-6) M, respectively, at day 3 (p < 0.001). Genistein at 10(-4) M increased the histamine content per 2 x 10(5) cells at day 3 from 5.9 +/- 1.2 micrograms/mL to 11.1 +/- 1.3 micrograms/mL (n = 6; p < 0.0001). These results indicate that genistein can inhibit proliferation and induce maturation of HMC-1 cells.
Allergy Asthma Proc
PMID:The isoflavone genistein inhibits proliferation and increases histamine content in human leukemic mast cells. 1461 39

The gastrointestinal tract is a rich source of mast cells with an enormous surface area that permits a high degree of interaction between the mast cell and the intestinal contents. The active metabolic products of the mast cell influence gastrointestinal secretion, absorption, and motility through paracrine effects of local mast cell activation and also cause systemic effects through the release of cellular products into the bloodstream. Recent advances in our knowledge of the immune system and the recognition that the gastrointestinal immune function might be partially mediated through gastrointestinal mucosal mast cells has opened mast cell research to the field of gastroenterology. Local gastrointestinal proliferation of mast cells in response to recognized or obscure stimuli can alter gastrointestinal function and induce systemic symptoms. Symptoms can arise from the increased number of mast cells, overproduction of specific mast cell mediators, and hyperactivity of the enteric nervous system that induces mast cell activation. The diseases mentioned in this review represent a small proportion of areas where mast cell function might play an important role in the response to disease and generation of symptoms.
Curr Allergy Asthma Rep 2004 Jan
PMID:The role of mast cells in common gastrointestinal diseases. 1468 Jun 22

Asthma is a common, chronic inflammatory condition of the airways that leads to airway hyperresponsiveness, reversible narrowing of the airways, and airway wall remodeling. Cytokines are involved in various aspects of asthma pathophysiology, such as the polarization of T-helper (Th)2 cells, antigen presentation, immunoglobulin (Ig)E response, airway wall remodeling, and mast cell and eosinophil recruitment and activation. Th2-derived cytokines, such as interleukin (IL)-4, IL-5 and IL-13 contribute to many of these aspects. Inhibition of individual cytokines for asthma therapy has been, and continues to be investigated. Anti-IL-5 monoclonal antibodies did not demonstrate beneficial effects in asthma, with only partial inhibition of eosinophilia in the airway wall; soluble IL-4 receptor, which neutralizes the effects of IL-4, has provided modest improvements in moderate asthma. The anti-IgE monoclonal antibody approach has demonstrated the most benefit in allergic asthma, particularly in severe disease. Which individual cytokine target can be inhibited with beneficial effects comparable to or above that of current inhaled corticosteroids can only be discovered through clinical trials. Blocking the effects of more than one cytokine may be more successful, and greater therapeutic effects may be observed in particular categories of asthma.
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PMID:Individual cytokines contributing to asthma pathophysiology: valid targets for asthma therapy? 1475 71

Mast cells are ancient, versatile immune effector cells. On the one hand, they are endowed with unique effector capabilities and activation responses that initiate innate immunity to bacteria and are essential to host defense against helminthic parasites. On the other hand, they are the major effector of type I hypersensitivity and an important participant in a number of disease processes. This review focuses on the mechanisms of mast cell development, the cytokine control of this process, and the amplification of mast cell effector systems as an important determinant of disease.
Allergy Asthma Proc
PMID:The biology of the mast cell. 1505 58


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