Allergic inflammation in the unified airway: start with the nose

It has long been recognised that there is an association between allergic inflammation in the upper airway (that is, allergic rhinitis) and in the lower airway (that is, allergic bronchitis or asthma). Indeed, up to 40% of patients with asthma have allergic rhinitis and vice versa.(1) Both conditions have similar immunological mechanisms and underlying pathogenesis(2 3) and, since one will affect the other, neither condition should be treated in isolation. Many theories have been postulated as to the link between allergic rhinitis and asthma. Given that the upper and lower airways do, after all, have the same epithelial lining, it is perhaps hardly surprising that each shows similar reactions to inhalant allergens and irritants. Another important factor is that patients with a blocked nose breathe through their mouth and consequently lose the air conditioning effect of normal nose breathing. Mouth breathing is normal only during speech and exercise. Asthmatic patients who mouth breathe are therefore exposing their tracheobronchial tree to cold dehumidified air which may aggravate bronchial hyperresponsiveness. The link between upper airway inflammation and asthma is not just confined to allergic rhinitis. Patients with nasal polyps are often non-atopic but commonly have associated asthma. Nasal polyposis, for example, occurs in 1% of the population but its frequency in patients with intrinsic asthma is 13% and in those with aspirin intolerance it has been shown to be 36%.(4) Patients with allergic rhinitis or polyps who do not have overt symptoms of asthma often exhibit underlying bronchial hyperresponsiveness, bronchial eosinophilia, or increased exhaled levels of nitric oxide(5-8).