Basic mechanisms of lung inflammation: executive summary of the first Lung Science Meeting of the European Respiratory Society at Taormina, Italy in 2003.

Abstract

The contribution of structural changes and the biology of lung cells to pulmonary disease was emphasised and contrasted with the inflammatory response at the first Lung Science Conference held at Taormina, Italy 26–28 March 2003 (table 1⇓). Here the basic mechanisms of inflammation and their relevance to lung diseases are discussed. For more information on the intracellular events discussed, look at and listen to individual talks on the European Respiratory Society web page at http://www.ersnet.org/taormina. View this table: 1 Central messages from Taormina Both the environment (“the air we breathe and the food we eat”) and the genetic potential (correct gene products expressed at the right place at the right time) contribute to homeostasis in the lung as well as to pathological deviation. Examples of environmental factors that contribute to the development of pulmonary disease were cigarette smoke condensate 1, lipopolysaccharide 2 and diesel exhaust particles. The redox potential of the lungs 3 is critical to the response to environmental insults and the subsequent expression of lung diseases 4. Genetic contributions to risk factors were discussed for sarcoidosis 5 and idiopathic fibrosis in surfactant protein (SP)‐D variants 6. A wound inflicted upon the pulmonary epithelium will attempt to heal. Concurrently, the immune system will respond with an inflammatory response to protect against imminent infection. Among the stimulating talks on repair, growth and differentiation of structural cells, the description of how embryos heal wounds 7, 8 was most fascinating. Using green fluorescent protein­labelled actin in drosophila and zebra fish, video sequences of differentiating embryos and wounded embryos showed how the epithelial cells stretch and pull toward each other in an attempt to close a wound. At the ends of the wound, lamellipodia of cells meet and interdigitate to reform the intact epithelium. If the drosophila homologue transforming growth factor (TGF)‐β PUK …