Abstract
The immunological and clinical parameters that are associated with asthma remission are poorly understood. The cytokine and local mediator changes associated with the resolution of asthma symptoms were examined in three groups of subjects 12–18 years of age (n = 15 in each group): (a) continuing asthma group (CA) who had persistent symptoms since early childhood, (b) an age, sex and atopic status-matched group who had persistent symptoms in early childhood but in whom these had resolved (RA), and (c) a non-atopic, non-asthmatic control group. Clinical parameters, sputum cell counts, peripheral blood mononuclear cell (PBMC) cytokine production and activation marker expression were determined. All of the CA had methacholine airway hyperresponsiveness compared with only half of the RA subjects. The CA showed elevated numbers of eosinophils and increased ECP and IL-5 in sputum, which were not observed in the RA. PBMC cytokine studies revealed increased production of the type 1 cytokines IL-12, IFN-γ and TNF-α in the CA group compared with the RA group, under a range of activation conditions, however, the production of IL-4 and IL-5 were unchanged. These findings suggest that decreased type 1 cytokine expression as well as decreased eosinophilic inflammation is associated with the resolution of asthma symptoms.
Highlights
Asthma is characterized by episodic symptoms of wheeze, breathlessness or chest tightness due to variable airflow obstruction and increased airway responsiveness that may or may not be associated with bronchitis
Increased levels of sputum eosinophils and sputum IL-5, increased peripheral blood mononuclear cell-derived TNF-α, IL-12, and decreased IFN-γ levels were associated with on-going asthma symptoms and airway hyperresponsiveness
We did not demonstrate any clear differences in T or B cell subsets, memory cells or activation markers between children with ongoing asthma symptoms and those in whom symptoms had completely resolved
Summary
Asthma is characterized by episodic symptoms of wheeze, breathlessness or chest tightness due to variable airflow obstruction and increased airway responsiveness that may or may not be associated with bronchitis. Sensitive individuals will respond with rapid mast cell degranulation and activation of antigen presentation, and the recruitment of effector cells such as T cells and eosinophils. This inflammatory response may become chronic, if allergen exposure is not terminated or if appropriate treatment is not administered. Chronically activated memory T cells are observed in asthma [16], with an enhanced capacity to produce IL-4 and IFN-γ [17,18] During this consolidation phase, structural damage due to persistent inflammation results in remodelling of the airways, leading to a degree of fixed airflow limitation and possibly greater hyperresponsiveness [19,20,21,22,23,24]
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