Airway remodeling in asthma.
OBJECTIVE
This overview summarizes some the more recent studies of remodeling in patients with asthma, studies using animal models to study the interaction of cell types and mediators, and studies using in vitro models to assess the effects of mitogenic stimuli, including mechanical strain, on mesenchymal cells and extracellular matrix proteins. The aim is to demonstrate how the term remodeling is becoming increasingly less specific as reductionism is applied to this field of study.


RESULTS
Specific areas of recent interest include plasticity of airway smooth muscle and fibroblast phenotype; the role of the extracellular matrix and its relation to the function of the airway smooth muscle and the mechanical properties of the airway wall; mitogenic stimuli arising from damaged epithelium, fibroblasts, smooth muscle cells, mast cells, eosinophils, and mechanical stress; extracellular and intracellular signaling in fibroblasts and smooth muscle cells; and therapeutic targets among the many pathways of remodeling-pathways that may be distinct from those involved in inflammation. The potential functional consequences of some of these findings call into question the role of remodeling. In some respects, it may represent a continuum from inflammation to scarring, but it may also be a protective response to altered airway mechanics caused by ongoing tissue damage or by abnormal airway structure present from early in life.


CONCLUSIONS
The diverse areas of research in this field are increasingly making the term remodeling as useful (or not) as the word asthma, because both can be used to describe simultaneously a large number of processes that may or may not be related to each other.
James
Alan
A
West Australian Sleep Disorders Research Institute, Queen Elizabeth II Medical Centre, School of Medicine and Pharmacology, University of Western Australia, Perth, Australia. ajames@it.net.au
D000818:Animals; D001249:Asthma / Q000473:pathology / Q000503:physiopathology*; D005347:Fibroblasts / Q000502:physiology; D006801:Humans; D007249:Inflammation / Q000503:physiopathology; D009130:Muscle, Smooth / Q000503:physiopathology; D012137:Respiratory System / Q000473:pathology / Q000503:physiopathology*