Introduction

Asthma is a clinical entity characterised by a combination of three features: airway obstruction with spontaneous and/or pharmacological reversibility, increased airway responsiveness (BHR), and airway inflammation.^1 2 Asthma originates with airway inflammation which results in the pathological process and ultimately culminates in symptoms.²

Airway inflammation has been considered the primary event leading to airway obstruction and hyperresponsiveness.² The principal pathological features of asthma include thickening and disorganisation of the tissues of the airway wall with epithelial shedding, deposition of collagen under the basement membrane, hypertrophy/hyperplasia of the smooth muscle, epithelial damage, occlusion of airways by secretion, and infiltration of eosinophils and T lymphocytes.¹ The investigation into the mechanisms involved in the pathogenesis of asthma has been hampered by difficulties in gaining direct access to asthmatic airways for evaluating the inflammatory process. Until recently it has not been possible in clinical practice to measure inflammation directly, and the presence or absence of . . . [Full text of this article]