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Biomedical subjects

H A Boushey

Publications and source records attributed to H A Boushey.

At least 19 recordsLinked to original sources
PubMed1996

Comparison of regularly scheduled with as-needed use of albuterol in mild asthma. Asthma Clinical Research Network.

BACKGROUND: Inhaled beta-agonists are the most commonly used treatment for asthma, but data suggest that regularly scheduled use of these agents may have deleterious effect on the control of asthma. We compared the effects of regularly scheduled use of inhaled albuterol with those of albuterol used only as needed in patients with mild chronic, stable asthma. METHODS: In a multicenter, double-blind study, we randomly assigned 255 patients with mild asthma to inhale albuterol either on a regular schedule (126 patients) or only as needed (129 patients). The patients were followed for 16 weeks. RESULTS: The primary outcome indicator, peak expiratory air flow measured in the morning, did not change significantly during the treatment period in the scheduled (416 liters per minute after the run-in period and 414 liters per minute after the treatment period) or the as-needed (424 liters per minute at both times) treatment groups (P=0.71). There were no significant differences between the two groups in peak flow variability, forced expiratory volume in one second, the number of puffs of supplemental albuterol needed, asthma symptoms, asthma quality-of-life score, or airway responsiveness to methacholine. The statistically significant differences between the groups in evening peak flow and in the short-term bronchodilator response to inhaled albuterol were small and judged to be clinically unimportant. CONCLUSIONS: In patients with mild asthma, neither deleterious nor beneficial effects derived from the regular use of inhaled albuterol beyond those derived from use of the drug as needed. Inhaled albuterol should be prescribed for patients with mild asthma on an as-needed basis.

Administration, Inhalation↗
PubMed1996

Exaggerated responses to chlorine inhalation among persons with nonspecific airway hyperreactivity.

Although chlorine gas is a common irritant exposure, little is known about airway responses to chlorine inhalation among persons with baseline airway hyperreactivity. We wished to determine whether such persons manifest an exaggerated response to chlorine compared with normal subjects. We studied 10 subjects, five with and five without airway hyperresponsiveness (HR) after exposure to 1.0 ppm chlorine and five persons, all with HR, to 0.4 ppm chlorine. After 1.0 ppm inhalation, there was a significant (p < 0.05) fall (mean +/- SE) in FEV1 immediately following exposure among normal (-180 +/- 37 mL) and HR subjects (-520 +/- 171 mL). The fall was greater among the HR compared with the normal subjects (p = 0.04). Specific airway resistance (Sraw) increased to a greater degree among the HR group compared with normal subjects (p = 0.04). Among all subjects (n = 10), the proportional change in FEV1 after 1.0 ppm chlorine correlated with baseline reactivity (Spearman rank correlation r = 0.64, p < 0.05). At 24-h follow-up, there were no significant chlorine-related pulmonary function deficits. After 0.4 ppm chlorine inhalation, there was no significant pulmonary function effect. These data indicated that persons with hyperreactive airways manifest an exaggerated airway response to chlorine at 1.0 ppm. This suggests that when large numbers of persons are exposed to chlorine, a susceptible subpopulation may acutely respond with a greater decrement in pulmonary function.

Adult↗
PubMed1995

Analysis of induced sputum after air and ozone exposures in healthy subjects.

Exposure of healthy subjects to ozone is associated with increases in cellular and biochemical markers of inflammation in bronchoalveolar lavage fluid. To determine if analysis of induced sputum might similarly reveal the pulmonary inflammatory effects of ozone exposure, we performed cellular and biochemical analysis of induced sputum collected 4 hr after air and ozone (0.4 ppm for 2 hr) exposures from 10 healthy subjects (age 30.0 +/- 5.0 years; 5 females) in a randomized crossover study in which exposures were separated by 2 weeks. We found that the total number of nonsquamous cells was significantly higher after ozone exposure than after air exposure (7.4 vs 3.9 x 10(5)/ml, P < 0.05) as was the percentage of the nonsquamous cells that were neutrophils (80.0 +/- 7.0% vs 51.0 +/- 20.0%, P < 0.05) and the levels of myeloperoxidase in the sputum fluid phase (1.6 +/- 0.6 vs 1.3 +/- 0.6 microg/ml, P < 0.05). In addition, IL-6 and IL-8 levels were higher after ozone than after air exposures, but not significantly so (44.5 +/- 32.4 pg/ml vs 26.8 +/- 30.7 pg/ml, P = 0.11; 1.5 +/- 0.5 ng/ml vs 1.1 +/- 0.6 ng/ml, P = 0.09). Mucin-like glycoprotein levels were also not significantly different between exposures (1.6 +/- 0.9 mg/ml vs 1.3 +/- 1.0 mg/ml, P = 0.26). We conclude that analysis of induced sputum is a useful noninvasive method for studying the pulmonary response to ozone exposure in healthy subjects.

Adult↗
PubMed1995

Prominent neutrophilic inflammation in sputum from subjects with asthma exacerbation.

To infer possible mechanisms of acute airway inflammation and mucus hypersecretion in acute severe asthma, we performed cellular and biochemical analysis on sputum from 18 adults with acute severe asthma and compared the results with results of analysis of sputum from 12 adults with cystic fibrosis (CF). We found that in subjects with asthma neutrophils made up more than 75% of sputum cells in 10 samples whereas eosinophils made up more than 75% of cells in only three samples. Fifty percent of the subjects with asthma reported that their asthma exacerbation was precipitated by a respiratory tract infection, and these subjects had a significantly higher percentage of neutrophils in their sputum (85% +/- 6% vs 57% +/- 12%, p = 0.05). In the CF samples neutrophils made up more than 95% and eosinophils less than 1% of cells in all samples analyzed. Analysis of fluid phase chemicals in asthmatic and CF sputum samples showed that despite overall lower mean values of neutrophil elastase (27 +/- 11 micrograms/ml vs 466 +/- 121 micrograms/ml, p = 0.0001) and interleukin-8 (IL-8) (55 +/- 15 ng/ml vs 186 +/- 24 ng/ml, p = 0.0001), some of the asthmatic samples had values for these variables that overlapped those in the CF samples. In addition, the asthmatic samples were distinguished by the presence of higher tryptase (10 +/- 7 U/L vs 0.9 +/- 0.9 U/L, p = 0.0001) and interleukin-6 (1166 +/- 447 ng/ml vs 186 +/- 24 ng/ml; p = 0.0001) levels and by a higher ratio of albumin to mucin-like glycoprotein (0.8 +/- 0.5 vs 0.1 +/- 0.002, p = 0.02). DNA levels were lower in the asthmatic samples (0.5 +/- 0.3 mg/ml vs 3.5 +/- 1.2 mg/ml, p = 0.05). We conclude that neutrophils predominate more frequently than eosinophils as the major inflammatory cell in sputum from patients with asthma in acute exacerbation. We speculate that this may be because respiratory tract infections are a frequent precipitant of acute asthma. In addition, the high IL-8 levels and free neutrophil elastase activity observed in asthmatic sputum suggests that IL-8 may mediate airway neutrophilia in acute asthma and that neutrophil elastase may mediate mucin glycoprotein hypersecretion in acute asthma, as has been proposed for the mucin hypersecretion in CF.

Adolescent↗
PubMed1995

Comparison of samples collected by sputum induction and bronchoscopy from asthmatic and healthy subjects.

To compare markers of inflammation in secretions obtained by sputum induction (SI), bronchial wash (50 ml instillate [BW]), and bronchoalveolar lavage (4 x 60 ml instillates [BAL]), we analyzed markers of inflammation in samples obtained by these methods in 10 healthy and 10 asthmatic subjects. Of the asthmatic subjects 8 had mild disease (FEV1, % of predicted > 75%). Within subjects from both groups, we found that sputum, compared with either BW or BAL, had higher numbers of nonsquamous cells (p = 0.0001) and higher levels of eosinophil cationic protein (ECP) (p = 0.0001), albumin (p = 0.0001), and mucin-like glycoprotein (p = 0.0001). The eosinophil percentages and the ECP levels in sputum correlated more closely with those in BW (r = 0.67, p = 0.005; r = 0.69, p = 0.0008, respectively) than in BAL (r = 0.5, p = 0.03; r = 0.37, p = 0.11). Comparing the asthmatic and healthy subgroups, we found that eosinophil percentages were higher in sputum (p = 0.0003) and BW (p = 0.006) from asthmatic subjects and that ECP levels were higher in BW (p = 0.001) and BAL (p = 0.0005) from asthmatic subjects. We conclude that analysis of induced sputum reveals information qualitatively similar to that obtained by analysis of BW and BAL and that sputum induction is not only noninvasive and easily repeated but also yields samples more concentrated and richer in airway secretions than those obtained by bronchoscopy.

Adult↗
PubMed1995

Effect of an NK1 receptor antagonist (CP-99,994) on hypertonic saline-induced bronchoconstriction and cough in male asthmatic subjects.

To investigate the role of NK1 receptors in the pathogenesis of bronchoconstriction and cough in asthma, we performed a randomized, double-blind, crossover study on the effects of a selective non-peptide tachykinin NK1 receptor antagonist (CP-99,994) on baseline measures of lung function and on hypertonic saline-induced bronchoconstriction and cough in 14 male subjects with mild asthma. CP-99,994 (250 micrograms/2 hours) and placebo were administered intravenously in 2-h infusions during consecutive visits 5 to 7 d apart. Specific airway resistance (SRaw) was measured and spirometry was performed at baseline and at 35 and 60 min. Next, hypertonic saline challenge was performed by delivering 10 breaths of saline of increasing concentration (0.9 to 7% in 1% increments at 5-min intervals) via an ultrasonic nebulizer until SRaw increased from baseline by 200% or 20 units, whichever was greater. Throughout the challenge cough was counted from a taped record made from two microphones placed close to the subject's larynx. We found that CP-99,994 did not significantly affect SRaw or spirometric measures of lung function during the first hour of infusion. Although CP-99,994 infusion markedly attenuated the bronchoconstrictor response to the saline challenge in two subjects, it did not significantly decrease the area under curves obtained for SRaw and cough during saline challenge for the group as a whole (p = 0.9 for SRaw;p = 0.8 for cough). We conclude that administration of 250 micrograms/kg of CP-99,994 over 2 h does not significantly inhibit hypertonic saline-induced bronchoconstriction or cough in subjects with mild asthma and does not have acute bronchodilator activity in these subjects.

Adult↗
PubMed1995

Basic mechanisms of asthma.

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.

Air Pollutants↗
PubMed1995

Pulmonary responses to purified zinc oxide fume.

BACKGROUND: Metal fume fever is a flu-like illness caused by zinc oxide fume inhalation and mediated by unknown mechanisms. It is one of a group of work-related febrile inhalational syndromes. We studied bronchoalveolar lavage (BAL) obtained from cigarette smoking and nonsmoking human volunteers after controlled exposure to purified zinc oxide fume to explore the possible roles of proinflammatory cytokines in this condition. METHODS: We studied 14 volunteers after inhalation exposure to purified zinc oxide fume and after sham exposure to air. The mean cumulative exposure was 537 +/- 232 mg min per cubic meter elemental zinc. Twenty hours after exposure we performed BAL. We analyzed BAL cells and studied BAL supernatant for cytokines including tumor necrosis factor-alpha (TNF alpha), interleukin(IL)-8, and IL-1 by enzyme-linked immunosorbant assay (ELISA). RESULTS: Polymorphonuclear leukocytes (PMNs) were significantly increased in the BAL fluid obtained post-exposure compared to sham (mean difference = 41.3 +/- 16.8 x 10(3) per mL; p < 0.05). Cumulative zinc exposure positively correlated with exposure-sham differences in BAL supernatant concentrations of both TNF (r2 = 0.58; p = .002) and IL-8 (r2 = 0.44, p = 0.01). Exposure-sham concentration differences in BAL supernatant IL-8 and BAL PMNs were also positively correlated (r2 = 0.60; p < 0.001). Cigarette smoking was not associated with exposure-sham differences in BAL TNF or IL-8, but did demonstrate a packs-per-day dependent increase in BAL supernatant IL-1 (t = 2.3, p = 0.04) post-exposure compared to sham, after taking into account the zinc exposure response. CONCLUSIONS: Purified zinc oxide fume inhalation causes an exposure-dependent increase in proinflammatory cytokines and PMNs in the lung. This supports a role for cytokine networking in mediating metal fume fever.

Adult↗
PubMed1995

Controversies involving inhaled beta-agonists and inhaled corticosteroids in the treatment of asthma.

Controversy over the use of inhaled beta-agonists has dated almost from their introduction as a treatment for asthma. Their effectiveness as bronchodilators is not disputed, but there is concern that they may worsen asthma control if used regularly and that excessive use may increase the risk of death from asthma. Five years after the report from Sears and colleagues suggested that regular use of fenoterol worsens asthma control, we do not have definitive corroborative evidence that this effect of fenoterol is real or is shared by other members of the beta-agonist class. It also remains disputed whether the documented association between excessive beta-agonist use and death from asthma is a causal or a spurious association. Undisputed is the fact that excessive beta-agonist use by asthmatics indicates an increased risk of death from asthma and so indicates a need for clinicians to advise anti-inflammatory medications for these patients. Happily, although there are legitimate concerns about the possible implications of the development of tolerance to the non-bronchodilating effects of beta-agonists, there is currently little evidence that treatment with conventional doses of the beta-agonists currently available in the United States, including salmeterol, is harmful to asthmatic patients. The controversies over the use of inhaled corticosteroids revolve around the issue of whether the clinical benefit easily demonstrated with their short-term use is justified in the face of their possible long-term systemic toxicity. Unsettled questions about their therapeutic use include whether dose dependence can be shown for the clinical benefits of inhaled corticosteroids, whether delay in initiating inhaled corticosteroid treatment reduces the benefit that can be achieved, and whether the benefits of even prolonged therapy are short-lasting. The great unsettled question about their toxicity is whether systemic absorption of inhaled corticosteroids increases the risk of long-term systemic complications, like osteoporosis, cataracts, and growth inhibition. Current evidence suggests that significant risk of such toxicity is not likely to be associated with the long-term use of the equivalent of 800 micrograms/d of beclomethasone in adults and 400 micrograms/d in children. If higher doses are used to obtain greater clinical benefit, the answers to these questions may determine the place of new inhaled corticosteroids with high local potency and little systemic activity.

Administration, Inhalation↗
PubMed1994

Analysis of induced sputum to examine the effects of prednisone on airway inflammation in asthmatic subjects.

To determine whether induced sputum samples might provide a useful means for evaluating the effects of therapy on airway mucosal inflammation, we examined induced sputum samples obtained before and after 6 days of treatment with prednisone (0.5 mg/kg/day) or placebo in a randomized, double-blind study of 24 asthmatic subjects. Induced sputum was analyzed for total and differential cell counts and for concentrations of eosinophil cationic protein, albumin, and mucin-like glycoprotein. We found that the mean (+/- SEM) percentage of eosinophils in sputum samples from the prednisone-treated group fell from 14.1% +/- 5.0% at baseline to 1.8% +/- 0.8% after treatment, a decrease significantly greater than in the placebo-treated group (from 10.3% +/- 4.9% to 11.1% +/- 4.0%; p = 0.002). The absolute number of eosinophils also decreased significantly more in the prednisone-treated group than in the placebo-treated group (p = 0.04). In addition, eosinophil cationic protein levels in induced sputum fell more in the prednisone-treated group than in the placebo-treated group (from 324 +/- 131 ng/ml to 144 +/- 84 ng/ml vs 173 +/- 50 ng/ml to 188 +/- 47 ng/ml; p = 0.002). Furthermore, prednisone treatment was associated with a significant increase in peak expiratory flow, an effect that was significantly correlated with the decrease in eosinophil percentage in induced sputum (rs = 0.64, p = 0.04). Prednisone treatment was not associated with any significant change in the concentrations of albumin or mucin-like glycoprotein. We conclude that analysis of induced sputum is a useful noninvasive method for studying the effects of asthma therapy on airway eosinophilic inflammation.

Adult↗
PubMed1994

Analysis of cellular and biochemical constituents of induced sputum after allergen challenge: a method for studying allergic airway inflammation.

To determine whether analysis of the constituents of induced sputum permits detection of changes provoked by aerosolized antigen challenge, we performed sputum induction (20-minute inhalation of aerosolized 3% saline solution) before and after aerosolized allergen challenge in eight subjects with asthma. Total cell counts and cell differentials of nonsquamous cells in induced sputum samples were determined after the samples were homogenized in dithiothreitol. Centrifugation of the entire homogenized sputum sample yielded supernatant that could be analyzed for biochemical constituents. We found that the median percentage of eosinophils and neutrophils in induced sputum samples was significantly higher 4 hours after allergen challenge neutrophils in induced sputum samples was significantly higher 4 hours after allergen challenge than at baseline (12% vs 0.5%, p < 0.05; 30.5% vs 7.5%, p < 0.05) and remained high 24 hours after challenge. Median levels of eosinophil cationic protein and histamine in induced sputum supernatants were significantly higher 4 hours after challenge than at baseline (151.3 vs 39.8 ng/ml, p < 0.05; 19.4 vs 8.8 micrograms, p < 0.05) and remained significantly higher 24 hours after challenge. Tryptase was detectable in sputum from seven of the subjects, and in these subjects, we found a trend toward an increase in median tryptase levels 4 hours after allergen challenge (4.4 vs 2.2 U/L, p = 0.09). We conclude that analysis of induced sputum after aerosolized allergen challenge reveals changes in inflammatory cells and markers similar to those reported in bronchoalveolar lavage fluid and that sputum induction is a useful noninvasive method for studying allergic airway inflammation in asthma.

Administration, Inhalation↗
PubMed1993

Cytokines in metal fume fever.

Metal fume fever is a flulike illness caused by zinc oxide inhalation and accompanied by an impressive pulmonary cellular response. We hypothesized that the syndrome is mediated by cytokines released in the lung after exposure to zinc oxide fume. We carried out 26 experimental welding exposures in 23 volunteer subjects, performing postexposure bronchoalveolar lavage (BAL) 3 h (n = 6), 8 h (n = 11), or 22 h (n = 9) after exposure. We detected tumor necrosis factor (TNF), interleukin-6 (IL-6), and interleukin-8 (IL-8) varying in a time- and exposure-related manner. The concentration of TNF in the BAL fluid supernatant was significantly greater at 3 h than at 8 h or 22 h after exposure (p < 0.05), exhibiting a statistically significant exposure-response relationship to airborne zinc at each follow-up time period (p < 0.05). TNF concentrations were statistically correlated with those of IL-6 in BAL supernatant obtained at 22 h (r = 0.78, p = 0.01) and with concentrations of IL-8 in BAL 8 h after exposure (r = 0.85, p = 0.001). IL-6 displayed a significant exposure-response relationship to zinc (p < 0.05) at 22 h. IL-8 exhibited a significant exposure-response relationship to zinc (p < 0.05) at 8 h after exposure, a time at which IL-8 correlated with marked increases in BAL fluid polymorphonuclear leukocytes (PMN) (r = 0.7, p = 0.01). Although we also detected interleukin-1 (IL-1) in BAL samples, this cytokine did not demonstrate a statistically significant exposure response. TNF, IL-6, and IL-8 in BAL fluid supernatant concentrations increased in a time and exposure-dependent fashion after zinc oxide welding fume exposure. The time course of increased cytokines, their correlations with one another and with PMN in the BAL fluid, and the consistency of our findings with the known kinetics and actions of these cytokines support the hypothesis that a network of cytokines is involved in the pathogenesis of metal fume fever.

Adult↗
PubMed1993

Cellular and biochemical analysis of induced sputum from asthmatic and from healthy subjects.

To determine the feasibility of cellular and biochemical analysis of sputum induced after inhalation of hypertonic (3%) saline, we analyzed sputum induced in 10 healthy and in 18 asthmatic subjects. We also analyzed saliva samples from all subjects. The entire sputum sample and the saliva sample were reduced using dithiothreitol, and cell counts and differentials were determined. Biochemical analysis was performed on sputum and saliva supernatants obtained after centrifugation. We found that induced sputum from asthmatic subjects had a higher percentage of eosinophils [8.1 +/- 3.43 (mean +/- SEM) versus 0.03 +/- 0.02%, p < 0.009] (after excluding squamous cells) and also had higher levels of albumin (232.3 +/- 54.8 versus 79.5 +/- 9.7 micrograms/ml, p < 0.02), fibrinogen (44.2 +/- 11.6 versus 11.9 +/- 2.5 micrograms/ml, p < 0.008) and eosinophil cationic protein (ECP) (142.6 +/- 34.2 versus 26.1 +/- 4.7 ng/ml, p < 0.006) but not of histamine or tryptase. In saliva, squamous cells made up more than 99% of the cells in both groups, and protein concentrations were not significantly different. We conclude that cellular and biochemical analysis of induced sputum is feasible in healthy and in asthmatic subjects and that it reveals differences similar to those reported from analyses of bronchial lavage fluid.

Adult↗
PubMed1993

Markers of mucus secretion and DNA levels in induced sputum from asthmatic and from healthy subjects.

To determine whether markers of mucus secretion can be quantified in airway lining fluid from asthmatic and from healthy subjects, we measured levels of a mucin-like glycoprotein (MLG) and lactoferrin in sputum induced by inhalation of hypertonic (3%) saline in 18 asthmatic and in 10 healthy subjects. Because DNA, like mucin, contributes to the viscosity of airway secretions, we also measured DNA levels in the induced sputum samples. To control for the presence of saliva in sputum, we also analyzed saliva samples from all subjects. The entire sputum sample and the saliva sample were reduced using dithiotreitol, and biochemical analysis was performed on supernatants obtained after centrifugation. We found that induced sputum from asthmatic subjects had higher levels of MLG [2,574.4 +/- 907.8 (mean +/- SEM) versus 562.2 +/- 90.5 micrograms/ml, p < 0.007] and DNA (7.1 +/- 1.6 versus 3.6 +/- 0.6 micrograms/ml, p < 0.05), but the difference in lactoferrin levels failed to reach statistical significance. However, in the subgroup of asthmatic subjects who gave a history of sputum production (n = 9), lactoferrin levels were higher than in the healthy control subjects (118.9 +/- 46.3 versus 35.2 +/- 6.5 micrograms/ml, p < 0.05). The very low levels of MLG, DNA, and lactoferrin measured in saliva were not significantly different in asthmatic subjects from those in healthy subjects. We conclude that measurement of markers of mucus secretion in induced sputum is feasible in asthmatic and healthy subjects, and it reveals abnormally high markers of mucus secretion in subjects with stable asthma.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Mucus hypersecretion in bronchiectasis. The role of neutrophil proteases.

To investigate the role of neutrophil proteases in the pathogenesis of mucus hypersecretion in bronchiectasis, we collected sputum samples from seven patients with bronchiectasis and measured their secretagogue activity by examining secretion of radiolabeled macromolecules by bovine airway submucosal gland cells incubated with sputum supernatants. There was marked secretagogue activity in bronchiectasis sputum, reaching a maximum of 1,963 +/- 292% (mean +/- SEM) above baseline at 1:15 dilution. Addition of ICI 200,355 (10(-5) M), a selective human neutrophil elastase inhibitor, decreased the secretory response markedly (72.53 +/- 5.89% reduction). The combination of aprotinin, an inhibitor of cathepsin G, and ICI 200,355 caused significantly more reduction in the secretory response than ICI 200,355 alone (89.12 +/- 3.8 versus 72.53 +/- 5.89% reduction, p < 0.05). We conclude that bronchiectasis sputum causes a large secretory response from tracheal submucosal glands due mostly to neutrophil proteases.

Adult↗