Epithelium-fibroblast interactions in response to airway inflammation.
Dramatic changes to the architecture of the airway walls have been commonly described in the airways of patients with asthma, cystic fibrosis (CF) and chronic obstructive pulmonary disease (COPD). Much research has focused on how airway inflammation drives these structural changes, particularly in terms of the mechanisms/mediators that are involved, and a number of parallels are observed between the disease phenotypes. For example, the increased deposition of extracellular matrix (ECM) at focal sites in the airway wall is seen in asthma and all interstitial lung diseases that involve fibrosis. In addition, increased expression of a number of well characterized cytokines and growth factors, such as TGF-beta and epidermal growth factor (EGF) have been demonstrated in these diseases. However, the role of the lesser-known cytokines, including the leukaemia inhibitory factor (LIF) and other members of the IL-6 family of cytokines in the pathogenesis of airway remodelling and fibrosis is largely unknown. However, the use of genetic manipulation in vivo and more specific inhibitors/antibodies in vitro has now provided increasing evidence to support the hypothesis that a complex interaction exists between these cytokines, ECM and integrins in regulating the function of both epithelial cells and fibroblasts.
Asthma and Allergy Research Institute, Department of Medicine, University of Western Australia, Nedlands, Western Australia, Australia.
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D000818:Animals; D001249:Asthma / Q000276:immunology* / Q000473:pathology; D016207:Cytokines / Q000276:immunology; D005347:Fibroblasts / Q000276:immunology*; D006133:Growth Substances / Q000276:immunology; D006801:Humans; D016023:Integrins / Q000276:immunology; D008168:Lung / Q000166:cytology / Q000276:immunology*; D012038:Regeneration; D020545:Respiratory Mucosa / Q000276:immunology* / Q000293:injuries
D016207:Cytokines; D006133:Growth Substances; D016023:Integrins