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Inflammation and Treatment in Asthma and COPD

By James F. Donohue, MD, FCCP; and Jill A. Ohar, MD, FCCP

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Objectives

  1. Understand the similarities and differences in inflammatory cells in asthma and COPD.
  2. Distinguish the Dutch hypothesis from the British hypothesis concerning the pathogenesis of COPD.
  3. Describe the role of inhaled corticosteroids in asthma and COPD.
  4. Identify appropriate therapeutic targets in asthma and COPD.
  5. Choose appropriate anti-inflammatory agents and bronchodilators for asthma and COPD.

Key words

asthma; COPD; eosinophil; inflammatory cell; mast cell; Th1 lymphocytes; Th2 lymphocytes

Abbreviations

BDP = beclomethasone dipropionate; FP = fluticasone propionate; GOLD = Global Initiative for Chronic Obstructive Lung Disease; ICS = inhaled corticosteroid; IgE = immunoglobulin E; IL = interleukin; LAR = late-phase allergic response; LTB4 = leukotriene B4; MMP = matrix metalloprotease; PDE4 = phosphodiesterase-4; Th1 = subtype 1 helper T; Th2 = subtype 2 helper T; TNF-a = tumor necrosis factor

Asthma is a chronic respiratory disorder characterized by reversible airflow obstruction and bronchial hyperresponsiveness.1 The primary pathologic components of asthma are inflammation and smooth-muscle dysfunction. In some patients, chronic inflammation of the airways may also result in structural changes, or remodeling, characterized by cellular proliferation of smooth muscle, basement-membrane thickening and to a lesser extent, increased deposition of matrix proteins and mucous gland hypertrophy.2 The clinical consequences of inflammation are exacerbations and bronchial hyperresponsiveness. Similar consequences are seen in COPD, but the underlying profile of inflammatory cells differs.
Although the pathogenesis of asthma has not been fully determined, asthma in children and adults is frequently associated with atopy, an inherited propensity to produce abnormal amounts of immunoglobulin E (IgE) against common environmental antigens. IgE-induced activation of mast cells results in the release of proinflammatory mediators. Atopy is one of the strongest identifiable risk factors for developing asthma. For COPD, exposure to environmental irritants such as tobacco smoke is the strongest risk factor.

This review will examine the critical role of inflammation in the pathophysiology of asthma and COPD, including its impact on airway structure and function. In addition, effective management strategies that target the inflammatory process that underlies asthma and COPD will be discussed. The review will also comment on the Dutch hypothesis, which is a unifying explanation for both asthma and COPD.

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