© 2004 BMJ Publishing Group Ltd & British Thoracic Society
EDITORIAL
Inflammatory cells and airway dysfunction
Location, location, location: microlocalisation of inflammatory cells and airway dysfunction
Institute for Lung Health, University of Leicester, Division of Respiratory Medicine, Leicester, UK
Correspondence to:
Correspondence to:
Dr I D Pavord
Institute for Lung Health, Department of Respiratory Medicine, University Hospitals of Leicester, Groby Road, Leicester LE3 9QP, UK; ian.pavord@uhl-tr.nhs.uk
Role of inflammatory cell location in the pathogenesis of asthma, COPD, and cough
Keywords: inflammatory cells; microlocalisation; asthma; chronic obstructive pulmonary disease
| The first 150 words of the full text of this article appear below. |
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
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