Leukocyte adhesion and recruitment, and alpha-1-antitrypsin deficiency: a report from ATS 2001, May 18-23, San Francisco

The program at this year’s American Thoracic Society international conference included over 300 scientific and clinical symposia. In this report I have reviewed the data presented on two important areas of lung inflammation, namely leukocyte recruitment and alpha-1-antitrypsin deficiency. Highlights included work from a number of groups identifying the contribution of specific leukocyte adhesion molecules (CD18, CD11a and vascular cell adhesion molecule-1) which varied according to the site and nature of the initial inflammatory stimulus. In addition work was presented examining the contribution of various chemoattractants to the process of leukocyte recruitment in chronic obstructive pulmonary disease, with leukotriene B4 in particular appearing to play a major role. In alpha-1antitrypsin deficiency other molecules may also be important and work was presented demonstrating the pro-inflammatory potential of alpha-1-antitrypsin polymers in the lungs of these patients. These advances in the understanding of the basic mechanisms of inflammation will, in the future, allow the development of novel anti-inflammatory therapies for a variety of lung diseases.