Current perspectives on airway inflammation and remodelling in asthma and allergic rhinitis

Abstract

1 Division of Allergy, Department of Pediatrics. Nippon Medical School, Tokyo, Japan. Review Article Braz J Allergy Immunol. 2013;1(5):243-52. Current perspectives on airway inflammation and remodelling in asthma and allergic rhinitis Ruby Pawankar, MD, PhD, FRCP, FAAAI1 The development of AR and asthma requires an interaction between the environment, immune system and genetic susceptibility. While pollen-induced rhinitis is the most characteristic IgEmediated allergic disease, in perennial allergic rhinitis the allergic triggers are more continuous, and lead to ongoing inflammation. Several cells and mediators orchestrate and maintain this inflammation. Although histamine is still one of the major mediators of the allergic reaction, many other mediators produced by different cell types are involved. Thus, the intricate interaction amongst these mediators, cytokines, chemokines, neuropeptides, adhesion molecules and various cells in the form of a complex network leads to the development of specific symptoms and the non specific hyperreactivity of allergic rhinitis. Asthma is characterized by variable degrees of chronic inflammation and structural alterations in the airways which include epithelial denudation, goblet cell metaplasia, subepithelial thickening, increased airway smooth muscle mass, bronchial gland enlargement, angiogenesis, and alterations in extracellular matrix components, involving large and small airways. Chronic inflammation is thought to initiate and perpetuate cycles of tissue injury and repair in asthma, although remodeling may also occur in parallel with inflammation. While AR and asthma share several similarities in the inflammatory cell and mediator profiles and responses, remodeling as seen in asthma is not characteristic of AR. In asthma, the relationships of airway inflammation, remodeling and lung function are becoming better understood. A variety of inflammatory cells and structural cells play a role in orchestrating the inflammation and structural changes in asthma. Increased airway responsiveness is a surrogate marker of inflammation and may reflect the development of structural changes in the airways. Such persistent increased bronchial responsiveness indicates remodeling which is partly resistant to therapy.