Cambridge Journals Online

Review Article

Mechanisms in allergic airway inflammation – lessons from studies in the mouse

Bennett O.V. Shuma1a2, Michael S. Rolpha1a2 and William A. Sewella1a3 c1 a1 Immunology and Inflammation Research Program, Garvan Institute for Medical Research, Darlinghurst, New South Wales, Australia. a2 CRC for Asthma and Airways, Camperdown, New South Wales, Australia. a3 St Vincent's Clinical School, Faculty of Medicine, University of New South Wales, Sydney, Australia.

Article author query shum bo   rolph ms   sewell wa

Abstract

Asthma is a chronic inflammatory disease of the airways, involving recurrent episodes of airway obstruction and wheezing. A common pathological feature in asthma is the presence of a characteristic allergic airway inflammatory response involving extensive leukocyte infiltration, mucus overproduction and airway hyper-reactivity. The pathogenesis of allergic airway inflammation is complex, involving multiple cell types such as T helper 2 cells, regulatory T cells, eosinophils, dendritic cells, mast cells, and parenchymal cells of the lung. The cellular response in allergic airway inflammation is controlled by a broad range of bioactive mediators, including IgE, cytokines and chemokines. The asthmatic allergic inflammatory response has been a particular focus of efforts to develop novel therapeutic agents. Animal models are widely used to investigate inflammatory mechanisms. Although these models are not perfect replicas of clinical asthma, such studies have led to the development of numerous novel therapeutic agents, of which some have already been successful in clinical trials.

Correspondence:

^c1 Corresponding author: William Sewell, Immunology and Inflammation Research Program, Garvan Institute for Medical Research, 384 Victoria St, Darlinghurst, New South Wales 2010, Australia. Tel: +61 2 9295 8434; Fax: +61 2 9295 8404; E-mail: w.sewell@garvan.org.au