The Pathology of Asthma, With Special Reference to Changes in the Bronchial Mucosa

Abstract

The pathological features of 20 cases dying in status asthmaticus have been studied. In gross sections the lungs showed no emphysema, but mucus plugs in the air passages and focal areas of collapse were outstanding features. Five cases showed cystic bronchiectasis which was of a similar distribution to the focal areas of collapse, occurring in the upper lobes as commonly as in the lower lobes.Histologically, shedding of the ciliated bronchial mucosal cells was prominent and this is attributed to a transudation of oedema fluid from the submucosa. Areas of regeneration of the mucosa, with the presence of simple stratified epithelium, were seen frequently. The loss of the ciliated respiratory epithelium and the transudation of oedema fluid into the bronchial lumen, with interference with the action of the remaining ciliated cells, are considered to be the essential factors in the failure of clearance of the bronchial secretions in asthma. It is postulated that bronchospasm plays little or no part in the shedding of the bronchial mucosa or in the pathogenesis of the asthmatic attack.

Pulmonary vascular changes in asthma and COPD

“…Early histological studies of lung tissue taken at post-mortem from subjects who died of status asthmaticus demonstrated the presence of mucus plugs in airway passages, loss of ciliated respiratory epithelium, and thickening of BM, infiltration of eosinophils, oedema and ASM hypertrophy, now collectively termed 'airway remodelling' [4]. Further studies in subjects with asthma were the first to confirm that changes in the airway vasculature are associated with remodelling of the airway wall [7,8].…”

“…Asthma studies were the first to confirm that changes in the bronchial vasculature are associated with remodelling of the airway wall [4][5][6][7][8]. Thereafter, a number of studies reported the involvement of specific growth factors, such as fibroblast growth factor (FGF), transforming growth factor (TGF) β1 and vascular endothelial growth factor (VEGF), during vascular remodelling in asthma and COPD [9][10][11][12].…”

Airway smooth muscle cells: contributing to and regulating airway mucosal inflammation?

“…Cytokines also induce the secretory form of phospholipase A 2 from airway smooth muscle cells [24]. Cultured human airway smooth muscle cells express mRNA for enzymes of the 5-lipoxygenase pathway, including 5-lipoxygenase, epoxide hydrolase, leukotriene (LT)C 4 synthase and c-glutamyl transpeptidase, as well as receptors for LTB 4 and Cys-LT 1 receptors [25]. The expression of these enzymes and receptors was increased following exposure to human atopic serum or to IL-1b.…”

“…Morphometric studies of airway smooth muscle in asthma have demonstrated that there is an increase in airway smooth muscle mass which is accounted for by hyperplasia and also by hypertrophy [4,5]. Such an increase in airway smooth muscle mass could contribute to the exaggerated airway narrowing observed in asthma [6,8] and may result from the action of growth factors released during the chronic inflammatory process.…”

IL-5 and IL-5 receptor in asthma

“…The link between abnormal airway physiology and airway inflammation was initially suggested by the results of post-mortem studies of asthmatic lungs which documented the presence of an inflammatory infiltrate (Dunnill 1960). The use of fibreoptic bronchoscopy has allowed bronchial biopsies and lavage fluid to be examined in less severe asthmatics and in normal subjects.…”