Abstract

Allergic asthma (AA) is a complex disorder with heterogeneous features of airway hyperresponsiveness, inflammation, and remodeling. The increase of airway smooth muscle (ASM) mass is a fundamental component of bronchial remodeling in AA, yet the pathophysiological mechanisms and clinical outcomes associated with ASM modulation are still elusive. The objective of this study is to compare the expression level of β-dystroglycan (β-DG) in ASM in AA subjects and a healthy control group and to investigate the relationship between eosinophils and β-DG in ASM in patients with AA. Thirteen AA patients and seven control subjects were analyzed for the ASM area and eosinophil cells. Bronchial biopsies were stained by β-DG and eosinophil cationic protein (ECP) using immunohistochemistry. The proportion of ASM with β-DG staining was greater in those with AA than in the healthy control group (mean (95% CI) (28.3% (23.8–32.7%) vs. 16.4% (14.1–18.5%), P < 0.0001). The number of ECP positive cells was higher in patients with AA than in the control group (4056 (3819–4296) vs. 466 (395–537) cells/mm2P < 0.0001). In AA, the number of ECP positive cells was significantly correlated to the β-DG expression in ASM (r = 0.77, P = 0.002). There is an increased β-DG expression in ASM and a higher number of ECP positive cells in the bronchial biopsy of those with AA than those in the control group. The increased expression of β-DG in ASM in AA subjects correlates with the number of eosinophils, suggesting a role for this cell in airway remodeling in AA.

Highlights

  • Allergic asthma (AA) is a heterogeneous and chronic inflammatory disorder associated with airway hyperresponsiveness (AHR), airway remodeling, and subsequently declining airway function [1]

  • The number of eosinophils was higher in the tissue of patients with AA than in the healthy control group (Fig. 2, a and b)

  • Statistical analysis demonstrated a significantly higher expression of β-DG in Airway smooth muscle (ASM) (a) and Eosinophil cationic protein (ECP) positive cells (b) (mean 28.3% (23.8–32.7%) vs. 16.4% (14.1–18.5%)), 11.9% (7.2–14.6%), and 95% CI for ECP in AA 4058 (3819–4296) vs. 466 (395–537) cells/ mm2 (3592 (3392–3664) cells/mm2, respectively (P < 0.001) (Fig. 3)

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Summary

Introduction

Allergic asthma (AA) is a heterogeneous and chronic inflammatory disorder associated with airway hyperresponsiveness (AHR), airway remodeling, and subsequently declining airway function [1]. It is characterized by a history of variable and repetitive respiratory symptoms that vary over time and in intensity, reversible airflow obstruction, and bronchospasm [2]. The hallmarks of airway remodeling in asthma comprise structural modifications in the bronchial wall: epithelial damage, subepithelial fibrosis, goblet cell hyperplasia/enlargement, mucus plugging, smooth muscle cell hyperplasia and/or hypertrophy, excessive extracellular matrix production [5], and angiogenesis of the bronchial vasculature [6]. The expression of smooth muscle proteins can be used as a marker for myocyte function in bronchial biopsies taken from the airways, vasculature, or other hollow organs [12]

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