Background: Allergic asthma is associated with chronic airway inflammation and progressive airway remodelling. However,\r\nthe dynamics of the development of these features and their spontaneous and pharmacological reversibility are still poorly\r\nunderstood. We have therefore investigated the dynamics of airway remodelling and repair in an experimental asthma\r\nmodel and studied how pharmacological intervention affects these processes.\r\nMethods: Using BALB/c mice, the kinetics of chronic asthma progression and resolution were characterised in absence and\r\npresence of inhaled corticosteroid (ICS) treatment. Airway inflammation and remodelling was assessed by the analysis of\r\nbronchoalveolar and peribronichal inflammatory cell infiltrate, goblet cell hyperplasia, collagen deposition and smooth\r\nmuscle thickening.\r\nResults: Chronic allergen exposure resulted in early (goblet cell hyperplasia) and late remodelling (collagen deposition and\r\nsmooth muscle thickening). After four weeks of allergen cessation eosinophilic inflammation, goblet cell hyperplasia and\r\ncollagen deposition were resolved, full resolution of lymphocyte inflammation and smooth muscle thickening was only\r\nobserved after eight weeks. ICS therapy when started before the full establishment of chronic asthma reduced the\r\ndevelopment of lung inflammation, decreased goblet cell hyperplasia and collagen deposition, but did not affect smooth\r\nmuscle thickening. These effects of ICS on airway remodelling were maintained for a further four weeks even when therapy\r\nwas discontinued.\r\nConclusions: Utilising a chronic model of experimental asthma we have shown that repeated allergen exposure induces\r\nreversible airway remodelling and inflammation in mice. Therapeutic intervention with ICS was partially effective in\r\ninhibiting the transition from acute to chronic asthma by reducing airway inflammation and remodelling but was ineffective\r\nin preventing smooth muscle hypertrophy.
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