Small airway inflammation in asthma

Meri K Tulic,Pota Christodoulopoulos,Qutayba Hamid

doi:10.1186/rr83

Meri K Tulic, Pota Christodoulopoulos + Show 1 more

Open Access

https://doi.org/10.1186/rr83

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Journal: Respiratory research	Publication Date: Jan 1, 2001
Citations: 169	License type: cc-by

Affiliation: McGill University, Christie (Canada)

Abstract

Asthma was originally described as an inflammatory disease that predominantly involves the central airways. Pathological and physiological evidence reported during the past few years suggests that the inflammatory process extends beyond the central airways to the peripheral airways and the lung parenchyma. The small airways are capable of producing T-helper-2 cytokines, as well as chemokines, and they have recently been recognized as a predominant site of airflow obstruction in asthmatic persons. The inflammation at this distal site has been described as more severe than large airway inflammation. These findings are of great clinical significance, and highlight the need to consider the peripheral airways as a target in any therapeutic strategy for treatment of asthma.

Highlights

Asthma is a complex, chronic inflammatory lung disease that is characterized by epithelial shedding, airway smooth muscle hypertrophy and hyperplasia, overproduction of mucus, and airway inflammation
Using resected lung specimens from asthmatic and nonasthmatic patients who underwent thoracic surgery, we evaluated the inflammatory process throughout the entire length of the airways [4]
The numbers of CD4+ cells in the endobronchial lamina propria were higher than in the alveolar tissue, only alveolar tissue CD4+ lymphocytes correlated with the predicted lung function at 4.00 a.m. (r = –0.68) and with the number of activated alveolar eosinophils (EG2 positive; r = 0.66) [11]. In this same cohort of patients, nocturnal asthma (NA) was associated with reduced glucocorticoid receptor (GR)binding affinity, reduced proliferation of peripheral blood mononuclear cells and decreased responsiveness to steroids at 4.00 a.m. comcommentary review that expressed GR-β were CD3+ T lymphocytes and, to a lesser extent, eosinophils, neutrophils and macrophages [9]. Those results suggest that the increased number of GR-β-positive cells in the small airways in fatal asthma may be associated with steroid insensitivity, contributing to asthma mortality

Summary

Introduction

Chronic inflammatory lung disease that is characterized by epithelial shedding, airway smooth muscle hypertrophy and hyperplasia, overproduction of mucus, and airway inflammation. Our results have shown increased numbers of T cells (CD3+), total eosinophils (major basic protein positive) and activated eosinophils (EG2 positive) in both small (< 2 mm internal diameter) and large (> 2 mm internal diameter) airways from asthmatic patients when compared with those of control individuals (Figs 1 and 2). In this same cohort of patients, NA was associated with reduced glucocorticoid receptor (GR)binding affinity (indicated by an increased Kd), reduced proliferation of peripheral blood mononuclear cells and decreased responsiveness to steroids at 4.00 a.m. comcommentary review that expressed GR-β were CD3+ T lymphocytes and, to a lesser extent, eosinophils, neutrophils and macrophages [9] Those results suggest that the increased number of GR-β-positive cells in the small airways in fatal asthma may be associated with steroid insensitivity, contributing to asthma mortality. These radiolabelled drug deposition studies must be interpreted with caution, because the labelling process itself may alter the distribution properties of the inhaled steroid particles

Conclusion

Findings

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