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Role of inflammatory cell location in the pathogenesis of asthma, COPD, and cough
Most inflammatory mediators are rapidly inactivated once they leave the cell so that they act across distances of only a few microns. It is therefore likely that microlocalisation between inflammatory and structural cells is a fundamental organising principle of airway inflammation and repair.
Enthusiasm for the view that microlocalisation is important in obstructive airway diseases has been fuelled by studies which showed inflammatory cells within the airway smooth muscle in asthma and chronic obstructive pulmonary disease (COPD) but not in normal controls. In asthma the airway smooth muscle is infiltrated by mast cells, predominantly of the chymase positive phenotype. Mast cell numbers correlate inversely with airway responsiveness,1 which suggests that interactions between mast cells and smooth muscle cells are central in the development of the disordered physiology in asthma. The strength of this assertion is underpinned by the paucity of mast cells within the airway smooth muscle in eosinophilic bronchitis, a condition that presents with chronic cough and shares many of the immunopathological features of asthma but is not associated with airflow obstruction or airway hyperresponsiveness.1–3 Importantly, there is evidence that mast cells infiltrating the airway smooth muscle bundle are activated; a necroscopic study of fatal and non-fatal asthma has shown that there is a marked increase in mast cell degranulation in the airway smooth muscle in both the large and small airways.4
A recent study has investigated whether a similar …
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