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 Asthma, Airway Biology, and Allergic Rhinitis in AJRCCM 2000

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مُساهمةموضوع: Asthma, Airway Biology, and Allergic Rhinitis in AJRCCM 2000   الأحد مارس 09, 2008 8:28 am


Am. J. Respir. Crit. Care Med., Volume 164, Number 9, November 2001, 1559-1580
Asthma, Airway Biology, and Allergic Rhinitis in AJRCCM 2000
Division of Pulmonary and Critical Care Medicine, Loyola University of Chicago Stritch School of Medicine and Edward Hines, Jr., Veterans Affairs Hospital, Hines, Illinois
Risk Factors
To determine risk factors for the onset of asthma and allergic rhinitis, Plaschke and coworkers (222) analyzed data from 1,370 subjects. Onset of allergic rhinitis was associated with sensitivity to birch (OR 6.5), sensitivity to Parietaria (OR 7.4), pets (OR 3.0), and being female (OR 1.9). Onset of asthma was associated with allergic rhinitis (OR 4.9), sensitization to pets (2.4), and smoking (OR 3.0). Among atopics, onset of asthma was associated with allergic rhinitis (OR 5.7). Among nonatopics, onset of asthma was associated with rhinitis (OR 3.5) and smoking (OR 5.7). The authors conclude that risk factors for the onset of allergic rhinitis are sensitization to pollen and pets, and risk factors for onset of asthma are allergic rhinitis, sensitization to pets, and smoking.
In the transitional epithelium of the nose, ozone induces epithelial hyperplasia and mucous cell hyperplasia. To determine the role of neutrophils in causing these injuries, Cho and coworkers (223) used antiserum against neutrophils. Rats treated with the antiserum had 90% fewer circulating neutrophils than control rats. After 3 days of exposure to ozone, antiserum-treated rats had 89% fewer infiltrating neutrophils, 66% less stored mucosubstances, and 58% less mucous cells in the nasal transitional epithelium. Antiserum had no effect on ozone-induced epithelial cell proliferation or upregulation of mucin mRNA. The authors conclude that mucous cell metaplasia caused by ozone is dependent on neutrophils, whereas epithelial cell proliferation and mucin gene upregulation are independent of neutrophils.
Quality of Life
To determine the relative burden and interaction of asthma and allergic rhinitis on quality of life, Leynaert and coworkers (224) analyzed answers to the SF-36 questionnaire by 850 participants in the European Community Respiratory Health Survey. Subjects who had allergic rhinitis alone were more likely to report problems with social activities and poorer mental health than were subjects without allergic rhinitis or asthma. Subjects who had both asthma and allergic rhinitis experienced more physical limitations than did patients with allergic rhinitis alone. Asthma did not impair social or mental health in subjects with allergic rhinitis.
Inflammation and Hyperreactivity
To determine whether the respiratory epithelium of aspirin-sensitive and aspirin-tolerant patients with rhinosinusitis differ in local production of eicosanoids, Kowalski and coworkers (225) cultured epithelial cells from removed nasal polyps. Without stimulation, epithelial cells from 10 aspirin-sensitive patients generated about one-third the amount of prostaglandin E2 generated by the aspirin-tolerant patients. The nasal level of 15-hydroxyeicosetetraenoic acid (15-HETE) did not differ between the groups. This eicosanoid increased 3.6 times when the cells of aspirin-sensitive patients were incubated with aspirin; no such change occurred in the aspirin-tolerant patients. The authors conclude that the epithelial cells in nasal polyps of aspirin-sensitive patients have abnormalities in eicosanoid generation.
Because the link between airway inflammation and hyperresponsiveness is not clear, Sanico and coworkers (226) investigated the role of nerve growth factor as a mediator of increased sensorineural responsiveness. In 20 subjects with allergic rhinitis, concentrations of nerve growth factor protein were increased in nasal fluid and nerve growth factor mRNA was decreased in superficial nasal scraping. Nasal provocation with allergen produced an increase in nerve growth factor protein in nasal fluid in subjects with allergic rhinitis, but not in the controls; concentration of the protein did not change with histamine provocation. The authors conclude that expression and release of nerve growth factor in mucosa occurs in allergic rhinitis.
To elucidate the mechanism of mucous hypersecretion in allergic inflammation, Shimizu and coworkers (227) developed a rat model of nasal allergy consisting of hypertrophy and metaplasia of goblet cells in the nasal epithelium in response to ovalbumin exposure. In this model, mucus production was inhibited by dexamethasone and by an inhibitor of cysteinyl-leukotrienes; eosinophilic infiltration was inhibited by a histamine-1 antagonist, dexamethasone, and anti-rat neutrophil antiserum. Instillation of lipopolysaccharide induced intraepithelial mucus production, which was inhibited by dexamethasone, indomethacin, and anti-rat neutrophil antiserum; an antagonist of cysteinyl-leukotrienes had no effect. The authors conclude that cysteinyl-leukotrienes may have a role in antigen-mediated mucus production, that eosinophil infiltration does not relate to mucus production, and that different mechanisms control mucus production in allergic inflammation and endotoxin stimulation.
To compare mucosal inflammation in the upper and lower airways of patients with allergic rhinitis, Braunstahl and coworkers (228) studied eight grass pollen-sensitive patients with allergic rhinitis but free of asthma. Segmental bronchial provocation produced an increase in eosinophils in blood and in bronchial mucosa (both challenged and unchallenged regions) at 24 hours. Eosinophils and eotaxin-positive cells were increased in the nasal lamina propria, and expression of interleukin-5 was increased in the nasal epithelium. The challenge produced nasal and bronchial symptoms and impaired function of both. A challenge in eight healthy controls had no effect. The authors conclude that patients with allergic rhinitis develop blood eosinophilia and allergic inflammation of the nose after a segmental bronchial provocation.
To study the effect of a topical glucocorticoid on the response of the nasal mucosa to allergen challenge, Linden and coworkers (229) did a double-blind crossover trial in nine subjects with allergic rhinitis. Allergen challenge produced acute nasal symptoms, which peaked at 30 minutes and then tapered. Undiluted mucosal fluids from the nose revealed increased levels of granulocyte-macrophage colony-stimulating factor and interleukin-5 at 3, 5, 7, and 9 hours. Topical budesonide (256 µg), 30 minutes before the challenge, had no effect on the symptoms but inhibited the increase in mediators. The authors conclude that granulocyte-macrophage colony-stimulating factor and interleukin-5 are induced in a nonsymptomatic, late-phase response to nasal allergen challenge, and that this cytokine response is prevented by a single dose of budesonide.
To determine the influence of airway production of cytokines on the outcome of rhinovirus infection, Gern and coworkers (230) studied 22 subjects with allergic rhinitis or asthma. Experimental infection with rhinovirus 16 produced neutrophilia in blood, and increases in granulocyte colony-stimulated factor, interleukin-8, and neutrophils in nasal secretions. Granulocyte colony-stimulating factor in nasal secretions was correlated with nasal neutrophils (rs = 0.87) and blood neutrophils (rs = 0.69), and nasal neutrophils were correlated with interleukin-8 (rs = 0.75). Similar relationships were seen in sputum, but the levels were more modest. The ratio of interferon-gamma-to-interleukin 5 mRNA, an indicator of the balance between T-helper cell type 1 (Th1) and Th2-like cytokines, was inversely correlated with both the peak of cold symptoms (rs = 0.60) and with the time of viral clearance. The authors conclude that airway interleukin-8 and granulocyte colony-stimulating factor are closely associated with neutrophilic inflammation during rhinovirus infection, and the balance between Th1- and Th2-like cytokines may influence outcome of common colds.
To assess the effect of ipratropium bromide on the nose's ability to condition cold, dry air, Assanasen and coworkers (231) did a double-blind crossover study in healthy nonallergic subjects. Ipratropium (84 µg) was sprayed into the nose 15 minutes before inspiring cold, dry air from a nasal mask. The nasal conditioning capacity, calculated by measuring the temperature and humidity of air entering and leaving the nose, was increased by ipratropium. Ipratropium lessened the fall in nasal volume resulting from cold, dry air, but it did not alter the decrease in nasal surface temperature. The authors conclude that ipratropium bromide increases the ability of the nose to condition cold, dry air.
To assess the influence of nasal polyposis on pulmonary function, Lamblin and coworkers (232) followed 46 patients over 4 years. At baseline, 34% of the patients had asthma and 54% had bronchial hyperresponsiveness. All 46 patients were initially treated with topical glucocorticoids for 6 weeks, and 39% experienced a decrease in nasal symptoms. Intranasal ethmoidectomy was performed in the nonresponders. Despite improvement in nasal symptoms in both groups at 1 and 4 years, patients not responding to topical glucocorticoids had a decrease in FEV1 at 4 years. The authors conclude that patients with nasal polyposis unresponsive to topical glucocorticoids develop worsening airway obstruction.
Because the efficacy of specific immunotherapy in asthma is controversial, Grembiale and coworkers (233) did a double-blind trial in 44 subjects with both perennial rhinitis and bronchial hyperresponsiveness. One year after monodesensitization to Dermatophagoides pteronyssinus (house dust mite), subjects had a 2.9-fold increase in PD20 (the provocative dose of methacholine producing a 20% decrease in FEV1); at the end of 2 years, PD20 increased to 4-fold. Although 9% of subjects in the placebo group developed asthma, none of the immunotherapy subjects did. The authors conclude that specific immunotherapy decreases airway hyperresponsiveness in carefully selected subjects with allergic rhinitis.
In 14 patients with both allergic rhinitis and asthma, Wilson and coworkers (234) compared the efficacy of a 2-week course of an inhaled glucocorticoid (budesonide 400 µg) combined with an intranasal glucocorticoid (budesonide 200 µg) versus a histamine receptor antagonist (citirizine 10 mg orally) combined with a leukotriene receptor antagonist (montelukast 10 mg orally). Both treatments achieved equivalent improvements in peak flow. Bronchial hyperreactivity was improved with the histamine and leukotriene receptor antagonists, but not with the glucocorticoid combination. Exhaled nitric oxide was suppressed by glucocorticoids but not by the receptor antagonists. The authors conclude that combined mediator blockade and combined topical glucocorticoids were equally effective for controlling asthma in patients with both asthma and allergic rhinitis.
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Asthma, Airway Biology, and Allergic Rhinitis in AJRCCM 2000
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