Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The last decade has seen a marked increase in the number of otolaryngologists-head and neck surgeons who have been trained to perform rhinologic surgery. This includes both rhinoseptoplasty and endoscopic sinus surgery. A better understanding of the pathophysiology of rhinitis and sinusitis has also kept pace with this rapid expansion of surgical intervention. For example, significant advances have taken place in our knowledge of the local immune system in the nose, particularly in regard to mucosal and submucosal mast cells and the development of protective antibodies in the nasal mucosa against viral and bacterial infections. We have far more understanding of the complex innervation of the blood vessels and glands in the nasal mucosa and their receptors, and, most recently, a tremendous increase of scientific data has accumulated on the effect of neuropeptides on the nasal mucous membrane. It is imperative that rhinologic surgeons have an understanding and appreciation of the complex patterns of sensory and autonomic innervation of the nose to better evaluate the medical, allergic, and surgical treatment of acute and chronic rhinitis and sinusitis. This discussion will focus on recent advances in our understanding of the biochemical substances that are released by both the autonomic nervous system and the sensory nervous system in the nasal mucosa. The effect of these mediators on both vascular smooth muscle and the seromucinous glands of the nose will be considered. Finally, the dynamic interaction between the inflammatory mediators released by sensory nerves so-called tachykinins-- and the immune system and mast cell degranulation will be considered.
 ...
PMID:The role of autonomic nervous system and inflammatory mediators in nasal hyperreactivity: a review. 166 47

Various cells are associated with inflammatory events characteristic of atopic allergy and asthma. As well as T cells and eosinophils, mast cells, basophils, mononuclear phagocytes and platelets have all to be considered particularly as their mediators have potential for contributing directly to the features of bronchial asthma. Nevertheless, mast cell/T lymphocyte/eosinophil interactions may be of particular significance. For instance, the acute symptoms of allergy and asthma such as sneezing, bronchospasm and hives are believed to be largely the result of mediator release from mast cells whereas chronic symptoms (the result of allergic inflammation) can be explained on the basis of eosinophil-mediated tissue damage. Allergen is recognized directly by T cells. Specialized T cell subsets, possibly the Th2 equivalent, predominate in allergy and elaborate IL-4 (an essential co-factor for IgE production) and IL-5 which brings about terminal differentiation and activation of the eosinophil. Basic proteins derived from the crystalloid granule together with PAF and leukotrienes produce chronic wheeze, bronchial irritability, and might also be involved in permanent nasal blockage in chronic rhinitis. This general hypothesis is continually being tested. It is clearly important to identify precise molecular targets in allergy and asthma in order to construct therapeutic strategies.
 ...
PMID:T lymphocytes and their products in atopic allergy and asthma. 193 73

Histamine and heparin, both free and cellular, were assayed in the nasal mucosa of 11 atopic and 15 nonatopic patients undergoing turbinectomy for chronic rhinitis. There was no significant difference between the free and cellular histamine levels of the atopic and nonatopic patients. There was also no significant difference between the free heparin levels of atopic and nonatopic patients. Mean cellular heparin was, however, significantly greater in the nonatopic group. This finding, together with the results of mast cell counting, suggests either that in atopic patients heparin stores are already depleted prior to turbinectomy, or that in nonatopic individuals nasal mast cells contain an excess of heparin in nonreleasable stores.
 ...
PMID:Nasal histamine and heparin in chronic rhinitis. 340 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.
 ...
PMID:Mast cell degranulation in nasal polyps. 352 8

The vital role of inflammation in the induction and perpetuation of asthmatic responses is now a widely accepted concept. Effective management of asthma requires modulation of asthmatic inflammatory responses. Eosinophils play a critical role in producing inflammation within the asthmatic lungs. Serologic assessment of the level of eosinophilic cationic protein (ECP) may be useful in assessing the degree of activation of eosinophils in asthma and the effect of pharmacotherapy on activated eosinophils. Several clinical trials have noted that ECP levels fluctuate in direct relationship to the amount of ongoing bronchospasm and asthmatic inflammation. Modulation of inflammation in asthma can occur through pharmacologic means. Nedocromil sodium has been demonstrated to significantly affect both early-phase and late-phase inflammatory events including effects on mast cell activation and effects on eosinophil function. Nedocromil sodium has also been noted to affect production and activity of cytokines that are vital to the perpetuation of the asthmatic late-phase response. Unlike cromolyn sodium, nedocromil sodium inhibits late-phase inflammation even when administered after the early phase of the allergic response and has also been demonstrated to be a steroid-sparing agent in mild-to-moderate asthmatics who require inhaled beclomethasone. Modulation of the metabolism of arachidonic acid, thereby affecting levels of prostaglandins and leukotrienes, may be extremely useful in selective asthmatic patients. Those patients having aspirin sensitivity and chronic rhinitis associated with asthma seem to be particularly responsive to arachidonic acid metabolites. In such patients, use of aspirin desensitization may be considered. Newer anti-inflammatory agents being investigated as treatments for asthma include methotrexate, hydroxychloroquin, auronifin, and sulfonylureas, among others.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Mediator assays and modulation of inflammation in asthma: introduction. 779 58

Inhalation exposures can produce asthma and rhinitis by several mechanisms. Sensitization with the production of IgE specific for a substance can lead to symptoms on reexposure via mast cell degranulation and the release of inflammatory mediators. Some substances, known as environmental adjuvants, enhance the immune response to concomitant exposures with the environmental adjuvant. Respiratory irritants can lead to asthma and rhinitis through interaction with chemical irritant receptors in the airway, leading to release of substance P from sensory nerves and neurogenic inflammation. The reactive airways dysfunction syndrome is a chronic asthma-like syndrome resulting from a single acute exposure to a respiratory irritant, while the reactive upper-airways dysfunction syndrome is chronic rhinitis stemming from an irritant exposure. The dysregulation of neurogenic inflammation by chemical exposures may be an important mechanism in the toxic induction of reactive airways dysfunction syndrome and reactive upper-airways dysfunction syndrome and may play a role in understanding the sick building syndrome and the multiple chemical sensitivity syndrome.
 ...
PMID:RADS and RUDS--the toxic induction of asthma and rhinitis. 793 8