Airways inflammation in allergic subjects : responses to air pollution

Abstract

By studying the baseline characteristics of inflammation in the lower airways of allergic asthmatic and rhinitic individuals, followed by controlled diesel exhaust exposure and re-analysis of the inflammation, the studies presented in this thesis have attempted to shed light on the transition phase of asymptomatic inflammation to clinical asthma and the role that air pollution might play in augmenting this transition.

The first study characterises the cellular inflammation in the lower airways of non-asthmatic, asymptomatic allergic rhinitic subjects, comparing them to asthmatic individuals treated with either β2-agonists alone or with and inhaled corticosteroids and healthy controls.  As anticipated, asthmatic subjects treated with β2-agonists alone had increased numbers of eosinophils and mast cells compared to healthy subjects, while those asthmatics on inhaled corticosteroids had a statistically significant increase in neutrophils.  Subjects with allergic rhinitis had similar inflammatory changes in the lower airways to those detected in the asthmatics treated with β2-agonists alone, but important differences included a smaller increase in effector cells such a eosinophils and an additional increase in the total number of T lymphocytes - specifically in the sub-population of CD8⁺ T-suppressor lymphocytes.  The lack of asthmatic symptoms in the allergic rhinitic subjects may be a dose-dependent effect with insufficient inflammatory cells present to result in bronchoconstruction; or it may be as a result of the different ratio of CD4⁺/CD8⁺ T-cells, with the increase in CD8⁺ T-suppressor lymphocytes having a protective effect.

The second study undertaken in this thesis has demonstrated that the neutrophilic and mast cell inflammation still persists in the lower airways of healthy subjects 18 hours after diesel exhaust exposure in addition to an increase in the numbers of eosinophils.  However, subjects with asthma and allergic rhinitis failed to show increase inflammation in the bronchial biopsies, although allergic rhinitics did have an increase in neutrophils in the bronchial wash.

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