Increased Sputum IL-8 and IL-5 in Asymptomatic Nonspecific Airway Hyperresponsiveness

Betz, R.; Kohlhäufl, Martin; Kaßner, Gudrun; Müllinger, B.; Maier, Konrad; Brand, P. L. P.; Weber, Norbert; Häußinger, K.; Heyder, J.; Frankenberger, Marion

doi:10.1007/s004080000055

Cited by 26 publications

(22 citation statements)

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“…A functional impact of neutrophils is supported by the observation that the number of neutrophils in the bronchoalveolar space correlates with the degree of nonspecific bronchial hyperreactivity in patients with mild, as well as severe persistent, asthma [34,60]. In severe persistent asthma, the bronchoalveolar content of the neutrophilic enzyme myeloperoxidase (MPO) also correlates with the degree of nonspecific bronchial hyperreactivity [34].…”

Section: Accumulation Of Neutrophils and Lung Functionmentioning

confidence: 75%

“…In line with such a destructive action, the accumulation of neutrophils locally in upper and lower airways appears to be linked to the long-term course and exacerbations of several acute and chronic lung disorders, including acute respiratory distress syndrome (ARDS), asthma, bronchiectasis, chronic bronchitis, chronic obstructive pulmonary disease (COPD), cystic fibrosis (CF) and chronic lung allograft rejection . The accumulation of neutrophils in the airways can also be linked to functional anomalies such as nonspecific bronchial hyperreactivity, hypersecretion and cough, all of which are key characteristics of obstructive lung disease [59,60]. This evidence provides a solid rationale for focusing research on the role of mechanisms leading to accumulation of neutrophils in severe asthma and COPD.…”

Section: Accumulation Of Neutrophils In Lung Diseasementioning

confidence: 99%

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Neutrophils, interleukin-17A and lung disease

Lindén¹

2005

European Respiratory Journal

219

182

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It is now established that an excessive and sustained mobilisation of neutrophils is a hallmark of several chronic inflammatory lung disorders, including severe obstructive lung disease. This article reviews evidence that the cytokine interleukin (IL)-17A is a major orchestrator of sustained neutrophilic mobilisation.Current evidence suggests that IL-17A is produced by T-lymphocytes, and that it exerts an orchestrating effect on the accumulation and associated activity of neutrophils in the bronchoalveolar space indirectly, through an induced release of specific cytokines and colonystimulating factors in resident lung cells.Although the involvement of IL-17A in inflammatory lung disorders is supported by several recent studies, its causative role is still uncertain.However, the unique position of interleukin-17A at the interface between acquired and innate immunity puts this cytokine forward as an important signal for the reinforcement of host defence; it also implies that interleukin-17A may constitute a useful target for pharmacotherapeutic intervention.

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Section: Accumulation Of Neutrophils and Lung Functionmentioning

confidence: 75%

Section: Accumulation Of Neutrophils In Lung Diseasementioning

confidence: 99%

Neutrophils, interleukin-17A and lung disease

Lindén¹

2005

European Respiratory Journal

219

182

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“…36 Similarly, increased airway deposition of cigarette smoke derived particles could increase local toxicity and gradually worsen airway inflammation and dysfunction. There is evidence from studies in bronchial biopsies 41 and sputum markers 42 that, even in individuals with asymptomatic BHR, there are signs of active inflammation. The dose-response relation between the quantity of cigarettes smoked and BHR, 43 airway inflammation, 44 and the risk for COPD 45 are well known and overtly visible in daily clinical practice.…”

Section: Discussionmentioning

confidence: 99%

Bronchial hyperresponsiveness and the development of asthma and COPD in asymptomatic individuals: SAPALDIA Cohort Study

Brutsche

2006

Thorax

153

106

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Background: Bronchial hyperresponsiveness (BHR) is a common feature of asthma. However, BHR is also present in asymptomatic individuals and its clinical and prognostic significance is unclear. We hypothesised that BHR might play a role in the development of chronic obstructive pulmonary disease (COPD) as well as asthma. Methods: In 1991 respiratory symptoms and BHR to methacholine were evaluated in 7126 of the 9651 participants in the SAPALDIA cohort study. Eleven years later 5825 of these participants were reevaluated, of whom 4852 performed spirometric tests. COPD was defined as an FEV 1 /FVC ratio of ,0.70. Results: In 1991 17% of participants had BHR, of whom 51% were asymptomatic. Eleven years later the prevalence of asthma, wheeze, and shortness of breath in formerly asymptomatic subjects with or without BHR was, respectively, 5.7% v 2.0%, 8.3% v 3.4%, and 19.1% v 11.9% (all p,0.001). Similar differences were observed for chronic cough (5.9% v 2.3%; p = 0.002) and COPD (37.9% v 14.3%; p,0.001). BHR conferred an adjusted odds ratio (OR) of 2.9 (95% CI 1.8 to 4.5) for wheezing at follow up among asymptomatic participants. The adjusted OR for COPD was 4.5 (95% CI 3.3 to 6.0). Silent BHR was associated with a significantly accelerated decline in FEV 1 by 12 (5-18), 11 (5-16), and 4 (2-8) ml/year in current smokers, former smokers and never smokers, respectively, at SAPALDIA 2. Conclusions: BHR is a risk factor for an accelerated decline in FEV 1 and the development of asthma and COPD, irrespective of atopic status. Current smokers with BHR have a particularly high loss of FEV 1 .

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“…However, this was associated with an increased risk of developing newly diagnosed asthma or COPD [Brutsche et al 2006]. In addition, smoking is a risk factor for developing bronchial hyperresponsiveness, and bronchial hyperresponsiveness is associated with accelerated lung function decline [Rijcken et al 1993] with a significant interaction with smoking [Betz et al 2001]. Thus active smokers with asymptomatic bronchial hyperresponsiveness are more prone to accelerated lung function decline leading to COPD, especially with fetal or childhood exposure to smoking leading to incomplete airway growth [Peat et al 1987].…”

Section: Bronchial Hyperresponsivenessmentioning

confidence: 99%

Asthma and chronic obstructive pulmonary disease overlap: asthmatic chronic obstructive pulmonary disease or chronic obstructive asthma?

Slats

Taube

2015

Ther Adv Respir Dis

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Asthma and chronic obstructive pulmonary disease (COPD) are different disease entities. They are both clinical diagnoses, with diagnostic tools to discriminate between one another. However, especially in older patients (>55 years) it seems more difficult to differentiate between asthma and COPD. This has led to the definition of a new phenotype called asthma COPD overlap syndrome (ACOS). However, our understanding of ACOS is at a very preliminary stage, as most research has involved subjects with existing diagnoses of asthma or COPD from studies with different definitions for ACOS. This has led to different and sometimes opposing results between studies on several features of ACOS, also depending on the comparison with COPD alone, asthma alone or both, which are summarized in this review.We suggest not using the term ACOS for a patient with features of both asthma and COPD, but to describe a patient with chronic obstructive airway disease as completely as possible, with regard to characteristics that determine treatment response (e.g. eosinophilic inflammation) and prognosis (such as smoking status, exacerbation rate, fixed airflow limitation, hyperresponsiveness, comorbidities). This will provide a far more clinically relevant diagnosis, and would aid in research on treatment in more homogenous groups of patients with chronic airways obstruction. More research is certainly needed to develop more evidence-based definitions for this patient group and to evaluate biomarkers, which will help to further classify these patients, treat them more adequately and unravel the underlying pathophysiological mechanism.

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Increased Sputum IL-8 and IL-5 in Asymptomatic Nonspecific Airway Hyperresponsiveness

Cited by 26 publications

References 0 publications

Neutrophils, interleukin-17A and lung disease

Neutrophils, interleukin-17A and lung disease

Bronchial hyperresponsiveness and the development of asthma and COPD in asymptomatic individuals: SAPALDIA Cohort Study

Asthma and chronic obstructive pulmonary disease overlap: asthmatic chronic obstructive pulmonary disease or chronic obstructive asthma?

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