Asthma and COPD (chronic obstructive pulmonary disease) are a growing major health burden, which, despite improvements in disease management, still require new effective treatments. As our understanding of the cellular and molecular processes which govern respiratory diseases improves, the range of potential therapeutic targets increase. PI 3-kinases (phosphoinositide 3-kinases) are a family of closely related enzymes, which play pivotal roles in a diverse array of cellular mechanisms. In the present paper, we review the evidence for PI 3-kinase involvement in various cellular processes underlying asthma and COPD generated through inhibitor studies and gene-targeting approaches, and discuss the prospects for PI 3-kinase inhibition as a future therapeutic strategy for the treatment of respiratory disease.

Abbreviations used: ARDS, acute respiratory distress syndrome; Bad, Bcl-2/Bcl-XL-antagonist, causing cell death; Bcl-2, B-cell leukaemia/lymphoma 2; COPD, chronic obstructive pulmonary disease; EPO, eosinophil peroxidase; fMLP, N-formylmethionyl-leucylphenylalanine; GM-CSF, granulocyte/macrophage-colony-stimulating factor; GPCR, G-protein-coupled receptor; IL, interleukin; ITAM, immunoreceptor tyrosine-based activation motif; PH, pleckstrin homology; PI 3-kinase, phosphoinositide 3-kinase; PLC, phospholipase C; PTEN, phosphatase and tensin homologue deleted on chromosome 10; SH2, Src homology 2; SHIP, SH2-containing inositol 5´-phosphatase; TNFα, tumour necrosis factor-α.

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Author notes

PI-3 Kinase in Signalling and Disease, a Biochemical Society Focused Meeting held at Novartis Horsham Research Centre, U.K., 11–12 November 2003