Increased levels of nitric oxide derivatives in induced sputum in patients with asthma

Kanazawa, Hiroshi; Shoji, Seiichi; Yamada, Masashi; Fujii, Takaaki; Kawaguchi, Takashi; Kudoh, Shinzoh; Hirata, Kazuto; Yoshikawa, Junichi

doi:10.1016/s0091-6749(97)70024-1

Cited by 69 publications

(55 citation statements)

References 28 publications

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“…KANAZAWA et al [19] showed a relationship between eosinophil count in the sputum and NO derivatives in asthmatic patients. Similarly, JATAKANON et al [1] showed a correlation between eosinophil percentage in the sputum and exhaled NO in asthmatic adults.…”

Section: Discussionmentioning

confidence: 99%

Neutrophil CD11b and soluble ICAM-1 and E-selectin in community acquired pneumonia

Glynn¹,

Coakley²,

Kilgallen³

et al. 1999

Eur Respir J

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Exhaled nitric oxide and eosinophil sputum markers are considered noninvasive ways in which to evaluate airway inflammation in asthma. The aim of this study was to evaluate the relationships between these methods of evaluation in asthmatic children.In a cross-sectional study of 25 mild±moderate asthmatic children (aged 6±13 yrs, 10 patients on inhaled steroids) exhaled NO was measured along with induced sputum by inhalation of hypertonic saline solution. The sputum was processed for eosinophil count and eosinophil cationic protein (ECP) determination. Serum ECP and lung function (forced expiratory volume in one second (FEV1)) were also measured.A significant correlation was observed between exhaled NO and sputum eosinophils (r=0.438, p=0.032) as well as between sputum eosinophils and sputum ECP (r=0.532, p<0.01). No correlation was observed among exhaled NO and serum ECP, sputum ECP, FEV1, respectively. Furthermore no correlation was observed between sputum eosinophil (%) and serum ECP and between sputum eosinophils and FEV1. There was no correlation among the investigated parameters in children treated with inhaled steroids.In conclusion, exhaled NO and sputum eosinophil counts are concordant in evaluating the degree of airway inflammation in patients with mild-to-moderate asthma. However, the association between these two noninvasive markers becomes less in steroid treated patients. Eur Respir J 1999; 13: 1386±1390.

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Section: Discussionmentioning

confidence: 99%

Neutrophil CD11b and soluble ICAM-1 and E-selectin in community acquired pneumonia

Glynn¹,

Coakley²,

Kilgallen³

et al. 1999

Eur Respir J

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“…Eosinophils in asthmatic airways also release leukotrienes, which cause contraction of airway smooth muscle and microvascular leakage. It has previously been shown that the degree of eosinophilic inflammation reflects the amount of toxic radicals produced in the airway which damage airway epithelium [17]. Accordingly, it is possible that bronchoconstriction, stimulated by various types of mediators from mast cells, is markedly potentiated in the presence of eosinophilic inflammation.…”

Section: Discussionmentioning

confidence: 99%

Severity of exercise-induced bronchoconstriction is related to airway eosinophilic inflammation in patients with asthma

Yoshikawa

Shoji²,

Fujii³

et al. 1998

Eur Respir J

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125

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Exercise-induced bronchoconstriction (EIB) is widely prevalent in asthmatic patients. Eosinophilic airway inflammation is considered to be a major factor in the pathogenesis of asthma. However, the effects of eosinophilic airway inflammation on EIB have been elucidated insufficiently. To examine the relationship between the severity of EIB and eosinophilic inflammation, sputum induction and exercise challenge were performed in 21 asthmatic patients. Significantly higher percentages of eosinophils and levels of eosinophil cationic protein (ECP) were found in induced sputum in EIB-positive asthmatics (median (range), eosinophils: 23.5 (11.0-61.0)%; ECP: 1,475 (74.8-17,701) ng x mL(-1)) than in EIB-negative asthmatics (eosinophils: 6.0 (1.0-41.5)% (p=0.006); ECP: 270.6 (10.8-7,700) ng x mL(-1) (p=0.049)). There was a significant correlation between the severity of EIB and the sputum eosinophil percentage (r=0.59, p=0.009) and the level of ECP (r=0.47, p=0.037). The area under the curve of the forced expiratory volume in one second for 30 min after exercise correlated with the percentage of eosinophils (r=0.60, p=0.008) and the level of ECP (r=0.45, p=0.04). There was no correlation between airway responsiveness to methacholine on the one hand and EIB, sputum eosinophils or ECP on the other. In conclusion, these results provide evidence that the severity of bronchoconstriction evoked by exercise is more closely related to eosinophilic airway inflammation than airway hyperresponsiveness to methacholine in asthmatic patients.

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“…Measurement of exhaled NO concentration may be clinically useful in detection and management of cytokine-mediated inflammatory lung disorders [6]. In particular, one set of results indicates that higher concentration of NO metabolites was found in induced sputum of patients with asthma as compared with normal subjects [9]. To our best knowledge, there have been no published data comparing changes of NO metabolites in induced sputum before and after the treatment.…”

Section: Introductionmentioning

confidence: 99%

Nitric oxide metabolites in induced sputum: a marker of airway inflammation in asthmatic subjects

Choi²,

et al. 1999

Clin Experimental Allergy

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SummaryBackground and objective The role of nitric oxide (NO) needs to be further clarified in allergic inflammation. This study was designed to investigate the relationships between NO metabolites and eosinophil count, eosinophil cationic protein (ECP), interleukin (IL)-5 in induced sputum from asthmatics. Methods Hypertonic saline-induced sputum was obtained in 25 asthmatic subjects, among which 13 patients were examined before and after anti-asthmatic medications including steroid preparations. Ten normal subjects were enrolled as controls. Fresh expectorated sputum separated from saliva was treated with equal volume of dithiothreitol 0.1%, cytospined for cell count, and the supernatant was collected for biochemical assay. NO metabolites were assayed by using modified Griess reaction. ECP was measured by fluoroimmunoassay, and detected IL-5 by a sandwich ELISA. Results Asthmatic subjects, compared with controls, had significantly higher concentration of NO metabolites (1035.4 Ϯ 125.3 vs 557.2 Ϯ 101.5 mmol/L, P < 0.01), higher percentage of eosinophils (25.6 Ϯ 4.6 vs 1.7 Ϯ 0.2%, P < 0.01), and higher levels of ECP (1117.8 Ϯ 213.9 vs 154.6 Ϯ 47.4 mg/L, P < 0.01) in the induced sputum. IL-5 was detected more frequently in asthmatic subjects than in control subjects (11/25 [44%] vs 1/10 [10%], P < 0.05). According to asthma severity, moderate to severe asthmatic subjects (n ¼ 18) had higher level of NO metabolites (1143.8 Ϯ 156.3 vs 575.5 Ϯ 89.5 mmol/L, P < 0.01), higher levels of ECP and IL-5 (P < 0.01, respectively) in the induced sputum than in those of mild asthmatic subjects (n ¼ 7). NO metabolites, the percentage of eosinophils, the levels of ECP, and IL-5 were reduced following treatment with anti-asthmatic drugs (P < 0.01, respectively). There were significant positive correlations between NO metabolites and percentage of eosinophils or ECP (r ¼ 0.34, P < 0.05; r ¼ 0.28, P < 0.05). Negative correlations were noted between FEV 1 , FEV 1 /FVC and proportion of eosinophils, ECP, or IL-5 levels. Conclusion These findings confirmed that the level of NO metabolites was increased in the tracheobronchial secretion of asthmatic subjects and was paralleled with severity of asthma. Measurement of NO metabolites in induced sputum may be used for monitoring the degree of airway inflammation in asthmatics.

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Increased levels of nitric oxide derivatives in induced sputum in patients with asthma

Cited by 69 publications

References 28 publications

Neutrophil CD11b and soluble ICAM-1 and E-selectin in community acquired pneumonia

Neutrophil CD11b and soluble ICAM-1 and E-selectin in community acquired pneumonia

Severity of exercise-induced bronchoconstriction is related to airway eosinophilic inflammation in patients with asthma

Nitric oxide metabolites in induced sputum: a marker of airway inflammation in asthmatic subjects

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