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)

Asthma is characterised by bronchial hyperresponsiveness. This feature of the asthmatic diathesis predisposes patients to wheezing in response to a number of different factors. These precipitating factors include specific allergen acting via sensitised mediator cells through an IgE-dependent mechanism. There are irritants which may work through a non-specific manner, or stimuli such as exercise and hyperventilation, which probably also act through mediator release via a non-IgE-dependent manner. The mechanism whereby physical stimuli such as exercise induce bronchoconstriction is of interest, because it increases the context in which the mast cell may participate in acute asthmatic bronchoconstriction. Respiratory infections also commonly provoke asthma, especially in infants and may, indeed, precipitate the asthmatic state itself. Finally, drugs can often trigger asthma attacks and the mechanisms of asthma precipitated by non-steroidal anti-inflammatory drugs such as aspirin have been the subject of recent research.
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PMID:Precipitating factors of asthma. 161 89

The methodology for isolating rat peritoneal mast cell was established. The main pathogenic bacterial ultrasonicates of respiratory infection in GuangZhou area have been examined for their ability to release histamine from purified rat peritoneal mast cells. The results were as following: (1) 7 pathogenic bacteria can cause direct release of histamine from rat mast cells. The most effective histamine releasers were P. mira (histamine release percent is 26.89% +/- 6.70%), Strep. Pneu (24.16% +/- 3.71%), E. Coli (20.40% +/- 4.83%) and K. Pneu (17.91% +/- 4.60%). (2) Histamine release initiated by bacterial ultrasonicates was completed within 30 minutes E. Coli differed from K. Pneu induced histamine release was independent of its dose. (3) The products of K. Pneu did not induce histamine release directly and bacterial hemolysin may play a potent role in bacteria-induced release of histamine. Our findings provide some evidence for mechanism by which respiratory bacterial infection can precipitate or exacerbate attacks of bronchial asthma.
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PMID:[Histamine release from mast cell induced by main pathogenic bacteria of respiratory infections in Guangzhou area]. 751 19

Results of studies of the epidemiology, physiology, histopathology, and cell biology of asthma have revised our conception of the disease. Epidemiologic studies have shown asthma to be an important cause of death, suffering, and economic hardship. Physiologic studies have shown that asthma is a chronic illness characterized by persistent bronchial hyperreactivity. Histopathologic studies have shown characteristic changes: epithelial damage, deposition of collagen beneath the basement membrane, eosinophilic and lymphocytic infiltration, and hypertrophy and hyperplasia of goblet cells, submucosal glands, and airway smooth muscle. Studies of the functions of cells in the airway mucosa suggest that asthma may be fundamentally mediated by a difference in the type of lymphocyte predominating in the airway mucosa but may also involve complex interactions among resident and migratory cells. Asthma may thus result from sensitization of a subpopulation of CD4+ lymphocytes, the Th2 subtype, in the airways. These lymphocytes produce a family of cytokines that favor IgE production and the growth and activation of mast cells and eosinophils, arming the airways with the mechanisms of response to subsequent reexposure to the allergen. This conceptual model has stimulated research along lines that will almost certainly lead to powerful new treatments, and it has already put current therapies in a new light, clarifying the role of antinflammatory agents, especially of inhaled corticosteroids. This conceptual model has some limitations: it ignores new evidence on the role of the mast cell in producing cytokines and depends on results of studies of the effects of inhalation of allergen, although most asthma exacerbations are provoked by viral respiratory infection. Preliminary studies suggest that viral infection and allergen inhalation may involve the activation of different pathways, with viral infection activating production of cytokines by airway epithelial cells. Similar study of the mechanisms activated by inhalation of air toxics may provide important clues as to how they might induce or exacerbate asthma.
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PMID:Basic mechanisms of asthma. 854 78

Respiratory infections are common causes of increased asthma for patients of all ages. Current evidence indicates that viral, and not bacterial, infections are the most important respiratory illnesses which increase the severity of asthma. Of the respiratory viral infections associated with increased asthma, rhinoviruses, i.e. the cause of common colds, have proven to be the virus most often found in association with increased asthma severity. Although the association between rhinovirus infections and asthma is most dramatically illustrated in children, asthma patients of all ages can be affected and the attacks of asthma can be severe. Studies to establish the mechanisms by which rhinoviruses enhance asthma severity have begun to focus on how this virus promotes allergic inflammation. We have found that experimental rhinovirus infections enhance airway responsiveness and, perhaps most importantly, the likelihood that a late allergic reaction will occur to an antigen challenge. Furthermore, using bronchoscopy and segmental antigen challenge, we have found that rhinovirus infections promote mast cell release of histamine and the recruitment of eosinophils to the airways. These data support the concept that rhinovirus infections act to promote allergic inflammation and by this mechanism increase both the likelihood of asthma occurring and the severity of wheezing.
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PMID:The role of respiratory viruses in asthma. 925 14

Immunosenescence is defined as changes in the innate and adaptive immune response associated with increased age. The clinical consequences of immunosenescence include increased susceptibility to infection, malignancy and autoimmunity, decreased response to vaccination, and impaired wound healing. However, there are several immune alterations that might facilitate persistence of asthma into late adulthood or development of asthma after the age of 50 to 60 years. Asthma in older patients is not uncommon, and this is a growing population as the average lifespan increases. Specific innate changes that might affect severity of asthma in older patients or be involved in the development of late-onset asthma include impaired mucociliary clearance and changes in airway neutrophil, eosinophil, and mast cell numbers and function. Additionally, age-related altered antigen presentation and decreased specific antibody responses might increase the risk of respiratory tract infections. Respiratory tract infections exacerbate asthma in older patients and possibly play a role in the pathogenesis of late-onset asthma. Furthermore, cytokine profiles might be modified with aging, with some investigators suggesting a trend toward T(H)2 cytokine expression. This review examines specific innate and adaptive immune responses affected by aging that might affect the inflammatory response in older adults with asthma.
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PMID:Age-related changes in immune function: effect on airway inflammation. 2092 Jul 59