Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Asthma is a chronic inflammatory disorder of airways. It is characterised by bronchoconstriction, oedema and airways mucus hypersecretion. The main clinical features of asthma are dyspnea, cough, wheezing and heaviness in the chest. The pathology of asthma is characterised by presence of many inflammatory mediators, where the most important are cysteinyl leukotriens. Leukotriens C4, D4 and E4 are 1000 times more potent than histamine in contracting airways smooth muscles. Inhibitors of arachidonic acid metabolism have been used in asthma treatment. They can block the 5-lipoxygenase enzyme and/or 5-lipoxygenase-activating-proteine (FLAP), or can block the cysteinyl leukotriene receptors on the cell surface. Many inhibitors of arachidonic acid metabolism have been found during experimental trials. But only two are used as a drugs: zafirlukast and montelukast (leukotriene receptor inhibitors) montelukast and zileuton (5-lipoxygenase inhibitors) having the best efficacy in asthma treatment. Chronic treatment with these drugs results in a decrease of asthmatic symptoms, improvement of lung function (FEV1, PEF) and decreased usage of other medications--beta-adrenergic agonists and inhaled steroids. It has been proved that zafirlukast and zileuton show the high efficacy in mild-to-moderate asthma, exercise-induced asthma, allergen-induced asthma and aspirin-induced asthma. These oral drugs have been shown to course only mild adverse effects (such as temporary elevation in liver function tests, gastrointestinel disturbances, headache). Clinical usage of zafirlukast, montelukast and zileuton is limited in our country, they are hardly approachable on the market and the cost of treatment is high.
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PMID:[The use of leukotriene receptor antagonists and 5-lipoxygenase inhibitors in bronchial asthma treatment]. 1010 12

Rhinovirus infections cause wheeze, cough, and bronchial hyperresponsiveness. To investigate the involvement of cysteinyl-leukotrienes and prostanoids in these symptoms, bronchial biopsy specimens from 9 normal subjects (nonatopic and with no history of chronic lung disease) were immunostained for 5-lipoxygenase (5-LO) and cyclooxygenase (COX) pathway enzymes 2 weeks before and 4 days after experimental infection with human rhinovirus serotype 16. 5-LO-positive cell counts increased 9-fold (from 0.48 to 4.4 cells/mm(2); P <.05), and 5-LO-activating protein (FLAP)-positive cell counts increased 3.6-fold (from 1.8 to 6.5 cells/mm(2); P =.09). Levels of leukotriene A(4) hydrolase and leukotriene C(4) synthase were unchanged. COX-2--positive cell counts increased from 0 to 2.6 cells/mm(2) (P =.009), with no change in COX-1 levels. Increases of 3-4-fold were seen in levels of macrophages (P =.02) and mast cells (P =.07) but not of eosinophils (P >.4), and bronchoalveolar lavage fluid cysteinyl-leukotriene levels doubled (from 11.2 to 20.4 pg/mL; P =.13). Cold symptom scores correlated with bronchial immunostaining for FLAP (rho = 0.93; P =.001). In normal subjects, rhinovirus colds induce bronchial inflammation with markedly enhanced expression of 5-LO pathway proteins and COX-2.
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PMID:Rhinovirus infection increases 5-lipoxygenase and cyclooxygenase-2 in bronchial biopsy specimens from nonatopic subjects. 1219 64