The relationship between inflammation and hyperreactivity of the airways in asthma

Chapman, Ian; Foster, A.; Morley, John E.

doi:10.1111/j.1365-2222.1993.tb00877.x

Cited by 63 publications

(26 citation statements)

References 37 publications

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“…One could therefore speculate whether a more aggressive treatment during the follow-up period would have resulted in higher lung function values and if these patients might benefit from an intensified ß 2 -agonist therapy rather than an increase in anti-inflammatory drugs [17]. This also supports the hypothesis that airway inflammation and hyperreactivity are sequential events and parallel systems where inflammation and bronchial hyperreactivity (BHR) can occur independently [18].…”

Section: G Kunkel and A-c Rydénsupporting

confidence: 55%

Serum eosinophil cationic protein (ECP) as a mediator of inflammation in acute asthma, during resolution and during the monitoring of stable asthmatic patients treated with inhaled steroids according to a dose reduction schedule

Kunkel

Rydén

1999

Inflammation Research

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Section: G Kunkel and A-c Rydénsupporting

confidence: 55%

Serum eosinophil cationic protein (ECP) as a mediator of inflammation in acute asthma, during resolution and during the monitoring of stable asthmatic patients treated with inhaled steroids according to a dose reduction schedule

Kunkel

Rydén

1999

Inflammation Research

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“…In particular there is no close relationship between the severity of airway inflammation, measured either by cell counts or NO in exhaled air, and either the severity of AHR or abnormalities in FEV " [15,28]. A large number of studies have now examined this relationship in endobronchial biopsies, sputum and bronchoalveolar lavage (BAL) and bronchial wash, and the literature is generally very consistent in showing at best a weak correlation.…”

Section: Asthma and Airway Inflammationmentioning

confidence: 87%

New insights into the relationship between airway inflammation and asthma

Wardlaw¹,

Brightling²,

GREEN³

et al. 2002

Clinical Science

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A B S T R A C TAsthma is a condition characterized by variable airflow obstruction, airway hyper-responsiveness (AHR) and airway inflammation which is usually, but not invariably, eosinophilic. Current thoughts on the pathogenesis of asthma are focused on the idea that it is caused by an inappropriate response of the specific immune system to harmless antigens, particularly allergens such as cat dander and house dust mite, that result in Th2-mediated chronic inflammation. However, the relationship between inflammation and asthma is complex, with no good correlation between the severity of inflammation, at least as measured by the number of eosinophils, and the severity of asthma. In addition, there are a number of conditions, such as eosinophilic bronchitis and allergic rhinitis, in which there is a Th2-mediated inflammatory response, but no asthma, as measured by variable airflow obstruction or AHR. Bronchoconstriction can also occur without obvious airway inflammation, and neutrophilic inflammation can in some cases be associated with asthma. When we compared the immunopathology of eosinophilic bronchitis and asthma, the only difference we observed was that, in asthma, the airway smooth muscle (ASM) was infiltrated by mast cells, suggesting that airway obstruction and AHR are due to an ASM mast cell myositis. This observation emphasizes that the features that characterize asthma, as opposed to bronchitis, are due to abnormalities in smooth muscle responsiveness, which could be intrinsic or acquired, and that inflammation is only relevant in that it leads to these abnormalities. It also emphasizes the importance of micro-localization as an organizing principle in physiological responses to airway inflammation. Thus, if inflammation is localized to the epithelium and lamina propria, then the symptoms of bronchitis (cough and mucus hypersecretion) result, and it is only if the ASM is involved -for reasons that remain to be established -that asthma occurs.

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“…The causative relationship between airway inflammation and hyperresponsiveness mayoften assumeseries pathology as shown in Fig. 3 but it may also assume parallel pathological processes (37). It is desirable that the causal relationship between inflammation and hyperresponsiveness of the airway is clarified in the future.…”

Section: Inflammation and Airway Hyperresponsivenessmentioning

confidence: 99%

Allergic Bronchial Asthma: Airway Inflammation and Hyperresponsiveness

et al. 2003

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The international consensus report on diagnosis and treatment of asthma was published in 1992 (Clin ExpAllergy 22: 1-72). According to the report, asthma is a chronic inflammatory disorder of the airways in which many cells play a role, including mast cells and eosinophils.Airway inflammation causes various symptoms of asthma which are usually associated with widespread but variable airflow obstruction and causes an associated increase in airway responsiveness to a variety of stimuli. The definition of asthma, provided in this report, is an epoch-making revision of the conventional recognition of asthma based on respiratory physiology and does not contradict the empirical knowledge that asthma responds well to steroid therapy. One reason, which led airway inflammation to be understood as a major factor in the pathophysiology of asthma is the technological advance and the widespread use of bronchoscopes. The use of bronchoscopyas a research tool has markedly improved the understanding of the pathology of asthma. It became also possible to link biopsy findings to autopsy findings in patients who died of asthma. However, it is relatively difficult to repeat a biopsy of the airway mucosal membranes in individual asthmatic patients. Here, animal models of asthma play a significant role. Findings from animal models can provide a clue for the development of new anti-asthmatic drugs. This paper will deal with the paradigm of allergic asthma and focus on recent topics of interleukin (IL)-4 and IL-5, which seem to play a central role in allergic asthma. The causative relationship between airway inflammation and hyperresponsiveness will be discussed. (Internal Medicine 42: 636-643, 2003)

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The relationship between inflammation and hyperreactivity of the airways in asthma

Cited by 63 publications

References 37 publications

Serum eosinophil cationic protein (ECP) as a mediator of inflammation in acute asthma, during resolution and during the monitoring of stable asthmatic patients treated with inhaled steroids according to a dose reduction schedule

Serum eosinophil cationic protein (ECP) as a mediator of inflammation in acute asthma, during resolution and during the monitoring of stable asthmatic patients treated with inhaled steroids according to a dose reduction schedule

New insights into the relationship between airway inflammation and asthma

Allergic Bronchial Asthma: Airway Inflammation and Hyperresponsiveness

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