Chest
Clinical Investigations: AirwaysStructural Changes of the Airway Wall Impair Respiratory Function, Even in Mild Asthma
Section snippets
Subjects
Subjects included 13 healthy nonatopic volunteers (control subjects, group 1), 26 patients with mild asthma treated with a bronchodilator alone without oral or inhaled corticosteroids or antiallergic agents (group 2), and 10 patients with mild-to-moderate asthma treated with inhaled corticosteroids and without oral steroids or antiallergic agents (group 3) [Table 1]. Asthma was diagnosed and classified according to the Guidelines for the Diagnosis and Management of the Asthma, Expert Panel
Subject Characteristics
Characteristics of the subjects, including age, sex, duration of asthma, dose of BDP, Rbm thickness, and respiratory function measurements in 13 healthy control subjects (group 1) and 36 patients with asthma (groups 2 and 3), are shown in Table 1; the characteristics of groups 2a and 2b are shown in Table 2. Patients with asthma in each group and healthy control subjects were similar in regards to age and sex.
Thickness of the Rbm in Patients With Mild Asthma and in Healthy Control Subjects
The Rbm was significantly thicker (mean ŷ SD) in patients with mild asthma not treated
Discussion
Patients with mild asthma have not had severe symptoms or severe airway inflammation. Most recent guidelines1,2,3,4 recommend that mild asthma be treated mainly with bronchodilators and without inhaled corticosteroids. However, we found that in patients with mild asthma not treated with inhaled corticosteroids, the Rbm was thicker than in healthy control subjects. Furthermore, we found that the Rbm was thicker than in healthy control subjects even in patients in whom mild asthma had been
Conclusion
We found that the Rbm was thicker in patients with mild asthma not treated with corticosteroids than in healthy control subjects or in patients with mild-to-moderate asthma intensively treated with inhaled corticosteroids. The thickening of Rbm correlated with the duration of asthma and with the impairment of respiratory function and airway hyperresponsiveness. These results suggest that treatment with inhaled corticosteroids should be started from the early stage of even mild bronchial asthma.
References (17)
- et al.
Remodeling of asthmatic airways by glucocorticosteroids
J Allergy Clin Immunol
(1996) - et al.
Bronchial subepithelial fibrosis correlates with airway responsiveness to methacholine
Chest
(1997) - et al.
Airways remodeling is a distinctive feature of asthma and is related to severity of disease
Chest
(1997) - et al.
Effect of early vs late intervention with inhaled corticosteroids in asthma
Chest
(1995) Standards for the diagnosis and care of patients with chronic obstructive pulmonary disease (COPD) and asthma
Am Rev Respir Dis
(1987)The British guidelines on asthma management: 1995 review and position statement
Thorax
(1997)Guidelines for the diagnosis and management of bronchial asthma
Allergology
(1995)
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Hydrogen sulfide inhalation ameliorates allergen induced airway hypereactivity by modulating mast cell activation
2015, Pharmacological ResearchCitation Excerpt :Accordingly, aerosol of hydrogen sulfide prevented FGF2 and IL-13 upregulation, that are known to activate lung fibroblasts in humans and in experimental animals [22,23]. In addition there is increasing evidence in humans for a strong correlation between sub-epithelial fibrosis and airway hyper-reactivity [24,25] as suggested by the increased numbers of fibroblasts/myofibroblasts found in the airways of asthmatic patients [26,27]. In order to address this issue we harvested fibroblasts from OVA-sensitized mice.
Diagnostic tools assessing airway remodelling in asthma
2012, Allergologia et ImmunopathologiaWhat effect does asthma treatment have on airway remodeling? Current perspectives
2011, Journal of Allergy and Clinical ImmunologyCitation Excerpt :Furthermore, TGF-β expression correlates with the degree of subepithelial fibrosis and is significantly increased in subjects with severe asthma with associated eosinophilia.22,23 RBM thickening is associated with many pathophysiologic features of asthma, can be found in subjects with all degrees of asthma severity,24,25 and correlates directly with airflow obstruction24,26 and AHR.27 Changes in RBM, in contrast, are negatively correlated with airway distensibility.12,28
TGFβ-induced matrix production by bronchial fibroblasts in asthma: Budesonide and formoterol effects
2011, Respiratory MedicineCitation Excerpt :Subepithelial fibrosis – thickened reticular basement membrane as a result of enhanced deposition of various extracellular matrix (ECM) molecules – is seen in airways of patients with asthma of all severities.1–5
The extra domain A of fibronectin is essential for allergen-induced airway fibrosis and hyperresponsiveness in mice
2011, Journal of Allergy and Clinical ImmunologyCitation Excerpt :Indeed, our model serves as an excellent tool to specifically evaluate the contribution of fibroblast activation and airway fibrosis to allergen-induced airway diseases. In line with our findings, a strong correlation between subepithelial fibrosis and AHR in response to methacholine or histamine has been reported in asthmatic subjects.29,30 Others found a correlation between AHR and ECM protein deposition by activated bronchial fibroblasts in asthmatic subjects.31
Effect of extracellular matrix composition on airway epithelial cell and fibroblast structure: Implications for airway remodeling in asthma
2009, Annals of Allergy, Asthma and ImmunologyCitation Excerpt :The RBM is significantly thickened even in mild forms of the disease10 and is phenotypically different from the normal BM. Reticular BM thickening is related to other airway remodeling changes and correlates with airflow limitation and AHR and is negatively correlated with airway distensibility.10–13 Although the normal airway BM is composed primarily of laminin, entactin, and collagen IV,14,15 the abnormal RBM consists predominantly of collagen I, collagen III, fibronectin, tenascin, laminin, and proteoglycans.16,17