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)

Currently, asthma therapies are effective in reducing inflammation but airway remodeling is poorly responsive to these agents. New therapeutic options that have fewer side effects and reverse chronic changes in the lungs are essential. This study aimed to determine the efficacy of oral administration of ginseng on lung histopathology in a murine model of chronic asthma. BALB/c mice were divided into four groups: control, placebo, ginseng, and dexamethasone. All mice except those in the control group were sensitized and challenged with ovalbumin. Then, mice in the ginseng group were given 2 gr/kg per day of ginseng and mice in the dexamethasone group received 1 mg/kg per day of dexamethasone via orogastic gavage once daily for 1 week. Lung histopathology was evaluated by using light and electron microscopy in all groups. All of the chronic changes of airways in the ginseng group were significantly ameliorated when compared with the placebo group. When compared with the dexamethasone group, the ginseng group had significantly lower numbers of mast cell count. Thicknesses of basement membrane, epithelium, and subepithelial smooth muscle were not statistically different between the ginseng and dexamethasone groups. Goblet cell numbers were much more reduced in the dexamethasone group. Ginseng is effective in resolving the established chronic histopathological changes of the lungs in the murine model of asthma.
Allergy Asthma Proc
PMID:Ginseng ameliorates chronic histopathologic changes in a murine model of asthma. 1861 6

Asthma is a chronic inflammatory disease of the airways characterized by variable airway hyperresponsiveness. Pharmacological therapy can include short acting beta2-agonists, low dose inhaled corticosteroids or long acting beta2-agonists, leukotriene modifying agents, anticholinergic bronchodilators, mast cell stabilizing medication and theophylline.
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PMID:Outpatient management of bronchial asthma in adults. 1868 Nov 6

Asthma is a chronic disease characterized by mast cell activation, mucus hypersecretion, airway obstruction, influx and activation of eosinophils, and generation of a predominant T-helper type 2-based cytokine environment. In individuals with established asthma, acute exacerbations requiring hospitalization result primarily from pulmonary viral infection, such as with influenza, rhinovirus, or respiratory syncytial virus. The mechanism for viral exacerbation of the asthmatic response is unclear, but evidence points to a key role for chemokines, a class of cytokines that are important in leukocyte recruitment, inflammatory cell activation, and T-cell differentiation. In this review, we focus on the chemokines upregulated in acute viral-induced exacerbation and examine their role in promoting the virus-induced pathophysiologic response in asthmatic individuals.
Curr Allergy Asthma Rep 2008 Sep
PMID:The role of chemokines in virus-associated asthma exacerbations. 1868 12

Asthma is a major cause of morbidity and mortality worldwide. It is characterized by airway dysfunction and inflammation. A key determinant of the asthma phenotype is infiltration of airway smooth muscle bundles by activated mast cells. We hypothesized that interactions between these cells promotes airway smooth muscle differentiation into a more contractile phenotype. In vitro coculture of human airway smooth muscle cells with beta-tryptase, or mast cells with or without IgE/anti-IgE activation, increased airway smooth muscle-derived TGF-beta1 secretion, alpha-smooth muscle actin expression and agonist-provoked contraction. This promotion to a more contractile phenotype was inhibited by both the serine protease inhibitor leupeptin and TGF-beta1 neutralization, suggesting that the observed airway smooth muscle differentiation was driven by the autocrine release of TGF-beta1 in response to activation by mast cell beta-tryptase. Importantly, in vivo we found that in bronchial mucosal biopsies from asthmatics the intensity of alpha-smooth muscle actin expression was strongly related to the number of mast cells within or adjacent to an airway smooth muscle bundle. These findings suggest that mast cell localization in the airway smooth muscle bundle promotes airway smooth muscle cell differentiation into a more contractile phenotype, thus contributing to the disordered airway physiology that characterizes asthma.
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PMID:Mast cells promote airway smooth muscle cell differentiation via autocrine up-regulation of TGF-beta 1. 1880 3

Gender differences in the development and prevalence of human diseases have long been recognized. Immense interest grows in the understanding of the role of sex hormones in the homeostasis of immunity. Asthma predominates in boys before puberty and this gender preference reverses after puberty and in adulthood, when adult women tend to have a more severe disease, often recalcitrant to treatment. Atopic eczema in preschool children shows insignificant gender difference or male preponderance in different studies, with more adult females suffering from atopic eczema. The limited data on the prevalence of immediate hypersensitivity to hymenoptera venom show controversial results. Discrepancy exists regarding the gender difference in food allergy, with females reporting significantly more allergic reactions in questionnaire studies. In general, adverse reactions to nonionic iodinated radiocontrast media are more commonly observed in females. The course of allergic diseases varies unpredictably during pregnancy, whereas hormone replacement therapy in postmenopausal women usually has a favorable influence on the course of asthma. Experiments in rodents confirm an effect of estrogens on mast cell activation and allergic sensitization, while progesterone is shown to suppress histamine release but potentiate IgE induction. Dehydroepiandrosterone may antagonize the production of Th2 cytokines but the effect of testosterone and the other androgens remains less defined. Actual data from human studies are lacking.
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PMID:Gender difference, sex hormones, and immediate type hypersensitivity reactions. 1892 78

Allergic conjunctivitis is an inflammatory condition of the ocular surface characterized by ocular itching, redness, tearing, chemosis, and eyelid swelling. The purpose of this study was to assess the comparative efficacy of an ophthalmic antihistamine/mast cell stabilizer solution and an intranasal steroid at reducing the signs and symptoms of allergic conjunctivitis induced by the conjunctival allergen challenge (CAC) model. Sixty subjects were enrolled in a single center, randomized, placebo-controlled, parallel-treatment, four-visit CAC study. After titration and confirmation of the allergic reaction at visits 1 and 2, subjects were randomized at visit 3 into one of 4 treatment groups (olopatadine 0.2% ophthalmic solution, fluticasone furoate nasal spray, a tear substitute, or saline nasal spray), dosed with study medication, and challenged 15 minutes later, after which ocular allergic signs and symptoms were assessed. Subjects continued treatment of the assigned medication for 6 days. At visit 4, subjects underwent similar procedures to those performed at visit 3. Fifty-nine subjects completed the study. Olopatadine 0.2% ophthalmic solution showed statistical and clinical superiority over fluticasone furoate nasal spray at all post-CAC time points after a single dose (p < 0.001) and after a 1-week loading period (p < 0.01) for ocular itching, the primary end point. Similarly, olopatadine 0.2% showed statistical and clinical superiority over fluticasone furoate for the majority of time points for ocular redness, tearing, chemosis, and eyelid swelling. Olopatadine 0.2% ophthalmic solution was statistically and clinically superior to fluticasone furoate nasal spray for the relief of signs and symptoms of allergic conjunctivitis.
Allergy Asthma Proc
PMID:A comparison of olopatadine 0.2% ophthalmic solution versus fluticasone furoate nasal spray for the treatment of allergic conjunctivitis. 1946 11

Mastocytosis is a rare disease characterized by an elevated whole body mast cell number. Anaphylaxis is a severe, generalized hypersensitivity reaction with rapid onset. The problem of anaphylaxis and mastocytosis is due to strongly increased mediator release from the elevated mast cell number during allergic reactions. This explains the much higher prevalence of anaphylaxis in mastocytosis than in the general population and its severe and sometimes fatal course. Because of the increased risk of anaphylaxis in mastocytosis, all patients with severe or recurrent anaphylaxis should be analyzed for underlying mastocytosis by estimation of baseline serum tryptase. If this is elevated, patients also should be tested via skin examination for cutaneous mastocytosis and with a bone marrow biopsy. All patients with mastocytosis and anaphylaxis must be instructed about avoiding the responsible elicitors and should carry an emergency kit with adrenaline for self-application. In mastocytosis patients with anaphylaxis due to Hymenoptera stings, venom immunotherapy is recommended for life.
Curr Allergy Asthma Rep 2009 Jan
PMID:The problem of anaphylaxis and mastocytosis. 1906 27

Chronic urticaria is a common heterogeneous condition that can be quite debilitating. There are a number of potential causes of urticaria, and the severity and clinical pattern can vary considerably from patient to patient. Eighty to 90% of patients with chronic urticaria have no specific external cause for their disease, which is therefore labeled "chronic idiopathic urticaria." We now know, however, that up to 30-50% of idiopathic cases may be autoimmune or related to mast cell and basophil abnormalities. There is evidence of an autoantibody to the high-affinity receptor for IgE (FcepsilonRI), specifically binding to the alpha-chain (FcepsilonRIalpha), which may be pathogenic. At this point in time, the gold standard for detecting clinically relevant autoantibodies to FcepislonRI is the functional in-vitro donor basophil histamine release assay. The exact prevalence and role of these autoantibodies is still under investigation. Histamine antagonists are the mainstays of therapy. For patients whose symptoms are not controlled by antihistamines alone, there are a number of adjunct therapy options, but there is still a need to develop better agents for this disease.
Allergy Asthma Proc
PMID:The spectrum of chronic urticaria. 1933 14

Asthma represents a syndrome of airway inflammatory diseases with a complex pathology. The immunologic pathogenesis is being increasingly revealed and provides opportunity for targeted biological intervention. This study was designed to describe current experience with immunomodulators as targeted therapy in asthma. A literature review was performed. Targeted therapies have included strategies to activate dendritic cells through the Toll-like receptor (TLR) 9 receptors, to interrupt the action of T(H)2 cytokines with cytokine blockers and monoclonal antibodies, to promote development of T(H)1 responses, to interrupt mast cell signaling, to block IgE mediated pathways, and to block TNF-alpha. Omalizumab is the only biological therapy that has an approved indication in asthma at this time. Improved understanding of the heterogeneity of asthma should allow for specific targeting of different disease phenotype-specific therapies including immunomodulators.
Allergy Asthma Proc
PMID:Immunomodulators in the treatment of asthma. 1946 1

Prior studies revealed the key roles played by T-helper type 1 and type 2 (Th1/Th2) cell dysregulation, IgE production, mast cell hyperactivity, and dendritic cell signaling in the evolution of the chronic, pruritic, inflammatory dermatosis that characterizes atopic dermatitis (AD). Accordingly, current therapy has been largely directed toward ameliorating Th2-mediated inflammation and pruritus. This article reviews emerging evidence that the inflammation in AD results from inherited and acquired insults to the barrier, as well as the therapeutic implications of this new paradigm.
Curr Allergy Asthma Rep 2009 Jul
PMID:Abnormal skin barrier in the etiopathogenesis of atopic dermatitis. 1965 72


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