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      Reticular basement membrane in asthma and COPD: Similar thickness, yet different composition

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          Reticular basement membrane (RBM) thickening has been variably associated with asthma and chronic obstructive pulmonary disease (COPD). Even if RBM thickness is similar in both diseases, its composition might still differ.


          To assess whether RBM thickness and composition differ between asthma and COPD.


          We investigated 24 allergic asthmatics (forced expiratory volume in one second [FEV 1] 92% predicted), and 17 nonallergic COPD patients (FEV 1 60% predicted), and for each group a control group of similar age and smoking habits (12 and 10 persons, respectively). Snap-frozen sections of bronchial biopsies were stained with hematoxylin/eosin and for collagen I, III, IV, V, laminin and tenascin. RBM thickening was assessed by digital image analysis. Relative staining intensity of each matrix component was determined.


          Mean (SD) RBM thickness was not significantly different between asthma and COPD 5.5 (1.3) vs 6.0 (1.8) μm, but significantly larger than in their healthy counterparts, ie, 4.7 (0.9) and 4.8 (1.2) μm, respectively. Collagen I and laminin stained significantly stronger in asthma than in COPD. Tenascin stained stronger in asthma than in healthy controls of similar age, and stronger in COPD controls than in asthma controls (p < 0.05).


          RBM thickening occurs both in asthma and COPD. We provide supportive evidence that its composition differs in asthma and COPD.

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          Characteristics of the inflammation in biopsies from large airways of subjects with asthma and subjects with chronic airflow limitation.

          Although the characteristics of the histopathologic changes present in subjects who die with status asthmaticus are well documented, the structural changes present in subjects with mild to moderately severe asthma are not well described and the inflammatory changes in the large airways of subjects with chronic airflow limitation (CAL) and asthma have not been compared. Ten subjects with asthma, five taking inhaled corticosteroids and five taking beta 2-agonist aerosols, five subjects with CAL, and four subjects with no respiratory illness had four biopsies taken from airways 10 mm in diameter. The length of intact epithelium, thickness of basement membrane, and number of lymphocytes, neutrophils, eosinophils, plasma cells, monocytes, and mast cells in the lamina propria, bronchial smooth muscle, and submucosa were measured. Intact epithelium was present along 56% of the basement membrane in the asthmatic subjects, along 54% in the subjects with CAL, and along 84% in the control subjects. In the asthmatic subjects there was no direct relationship between the severity of asthma and the amount of epithelial cell loss or the number of inflammatory cells. The basement membrane was thickened in all asthmatic subjects but not in normal subjects or subjects with CAL. There was a significant increase in the number of lymphocytes, eosinophils, and mast cells in the asthmatic airways, particularly in the lamina propria, compared with the CAL subjects. There were no eosinophils or mast cells in any of the control subjects. The airways of subjects with CAL contained significantly more inflammatory cells than the control subjects. Subjects with asthma on inhaled corticosteroids had significantly fewer lymphocytes, eosinophils, and mast cells compared with subjects taking only beta 2-agonists.(ABSTRACT TRUNCATED AT 250 WORDS)
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            Increased peak expiratory flow variation in asthma: severe persistent increase but not nocturnal worsening of airway inflammation.

            Asthma at night is characterized by a nocturnal increase in airway obstruction. It has been hypothesized that nocturnal asthma results from an increase in airway wall inflammation at night. However, studies on inflammatory cells in bronchoalveolar lavage (BAL) fluid and bronchial biopsies have produced conflicting data. This study assessed inflammatory cell numbers at 16:00 h and 04:00 h in bronchial biopsies of 13 healthy controls, 15 asthmatic patients with peak expiratory flow (PEF) variation 15%. There was no significant increase at night in the number of CD3, CD4, CD8, CD25, AAI (tryptase) and EG2-immunopositive cells in the submucosa in both groups. Numbers of EG2-positive cells in the two asthmatic groups were significantly higher than in healthy controls, both at 16:00 h (p 15% than in asthmatics with PEF variation 15% and 15% suffer from a higher overall severity of bronchial inflammation at night and during the day.
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              Structural changes of the airway wall impair respiratory function, even in mild asthma.

              To clarify whether structural changes of the airway wall impair respiratory function in patients with mild asthma, and to determine whether mild asthma should be treated with inhaled steroids. Showa University Hospital in Tokyo. Thirteen healthy nonatopic volunteers (control subjects), 26 patients with mild asthma treated with a bronchodilator alone without oral or inhaled corticosteroids or antiallergic agents, and 10 patients with mild-to-moderate asthma treated with inhaled corticosteroids. We measured the thickness of the epithelial reticular basement membrane (Rbm) of the airway wall in bronchial biopsy specimens from patients with asthma and from healthy control subjects. We also performed spirometry and histamine challenge tests to evaluate airflow obstruction and airway hyperresponsiveness. The thickness of the Rbm in patients with mild asthma was significantly greater than that in healthy control subjects and was negatively correlated with the FEV(1) as a percentage of FVC and the provocative concentration of histamine that caused a 20% decrease in FEV(1) from the post-saline solution baseline value. Moreover, the Rbm was thicker in patients with mild asthma not treated with inhaled steroids than in patients with mild-to-moderate asthma treated with inhaled steroids. The thickness of the Rbm is increased even in mild asthma and is correlated with airway obstruction and hyperresponsiveness. Our results suggests that anti-inflammatory treatment with inhaled steroids should be started in the early stage of bronchial asthma to prevent structural changes from occurring in the airway wall.

                Author and article information

                Int J Chron Obstruct Pulmon Dis
                International Journal of COPD
                International Journal of Chronic Obstructive Pulmonary Disease
                Dove Medical Press
                15 April 2009
                : 4
                : 127-135
                [1 ] Department of Pulmonology
                [2 ] Department of Pathology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands
                Author notes
                Correspondence: Nick H Ten Hacken Department of Pulmonology, University Medical Center Groningen, University of Groningen, Hanzeplein 1, 9713 GZ Groningen, PO Box 30001, 9700RB Groningen, The Netherlands, Tel +31 50 361 2357, Fax +31 50 361 9320, Email n.h.t.ten.hacken@
                © 2009 Liesker et al, publisher and licensee Dove Medical Press Ltd.

                This is an Open Access article which permits unrestricted noncommercial use, provided the original work is properly cited.

                Original Research


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