Airway hyperresponsiveness (AHR) is one of the hallmarks of asthma, which invariably correlates with the disease severity, and is defined as increased sensitivity and reactivity of the airways to numerous types of stimuli. Classically AHR is assessed by exposing patients to either “direct” stimuli, i.e. those that act directly on the airway smooth muscle such as histamine and methacholine, and “indirect” stimuli such as exercise, bradykinin and adenosine monophosphate that act via intermediary cells, such as mast cells and nerves. The exact mechanisms underlying AHR still remains to be fully determined, however, AHR can be divided into two types, acute and chronic AHR based partly on its response to inhaled corticosteroid (ICS) therapy. The acute type is thought to be due mainly to acute inflammatory changes such as mucus hypersecretion, airway wall edema and plasma leakage. This type of AHR responds well to ICS therapy. On the other hand, chronic AHR is thought to be due to airway wall remodeling such as fibrosis, smooth muscle hyperplasia/hypertrophy and airway nerve hyperalgesia. This type of AHR does not respond well to anti-asthma therapy when administered for many years. Whilst AHR remains a complex component of asthma, significant progress has been made in the last two decades that is slowly dissecting out the mechanisms of this characteristic feature of asthma.

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