Abstract
Airway inflammation is a key feature of upper and lower respiratory allergic diseases, such as allergic rhinitis and asthma. Characteristically, histological alterations such as goblet cell hyperplasia, mucus hypersecretion, loss of epithelial barrier function, airway infiltration and structural changes such as basal membrane thickening and airway smooth muscle hyperplasia. These inflammatory signs are often obvious already early in life and may be accompanied by structural changes (remodeling) occurring in early lifetime. This review focusses on the main mechanisms underlying the development of airway inflammation and remodeling and discusses the question which factors contribute to the persistence of airway inflammation in chronic allergic airway disease.
Highlights
Airway inflammation is a key feature of upper and lower respiratory allergic diseases, such as allergic rhinitis and asthma
It was commonly assumed that this allergic inflammation and its alternation with episodes of recovery would lead to structural changes, which are termed “remodeling”
This strictly sequential idea of early inflammation followed by structural remodeling has been questioned because current publications suggest very early structural changes in the pulmonary tissue in patients who later developed asthma; these structural changes were observed without the classic allergic inflammatory response
Summary
Airway inflammation is a key feature of upper and lower respiratory allergic diseases, such as allergic rhinitis and asthma. The classic and still valid model of the development of allergic airway inflammation assumes an early sensitization, which, after penetration by the allergen through the airway epithelium and the absorption of professional antigen-presenting cells (APCs), leads to the activation of type 2 T-helper cells (Th2).
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