Published ahead of print on November 19, 2004, doi:10.1165/rcmb.2004-0091OC
© 2005 American Thoracic Society DOI: 10.1165/rcmb.2004-0091OC Moraxella catarrhalis–Infected Alveolar Epithelium Induced Monocyte Recruitment and Oxidative BurstDepartment of Internal Medicine and Infectious Diseases, Charité–Faculty of Medicine, Humboldt- and Free University Berlin, Berlin; Department of Internal Medicine, Justus-Liebig-University Giessen, Giessen; and Department of Internal Medicine, Faculty of Clinical Medicine Mannheim, Ruprecht-Karls-University, Heidelberg, Germany Correspondence and requests for reprints should be addressed to Simone Rosseau, M.D., Department of Internal Medicine and Infectious Diseases, Charité–Campus Mitte, Schumannstrasse 20/21, 10117 Berlin, Germany. E-mail: simone.rosseau{at}charite.de
The recruitment of monocytes appears to be a crucial factor for inflammatory lung disease. Alveolar epithelial cells contribute to monocyte influx into the lung, but their impact on monocyte inflammatory capacity is not entirely clear. We thus analyzed the modulation of monocyte oxidative burst by A549 and isolated human alveolar epithelial cells. Epithelial infection with Moraxella catarrhalis induced monocyte adhesion, transepithelial migration, and superoxide generation, whereas stimulation with lipopolysaccharide, tumor necrosis factor-
Key Words: alveolar epithelial cells • monocytes • inflammation • lung • infection This article has been cited by other articles:
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, interleukin-1ß, or interferon-
induced adhesion or transmigration, but failed to initiate monocyte burst. The effect of microbial challenge was mimicked by phorbol myristate acetate and inhibited by the protein kinase C inhibitor bisindoylmaleimide. Furthermore, evidence for a role of platelet-activating factor–signaling in monocytes is presented. Monocyte burst was neither induced by supernatant nor affected by fixation of A549 cells, excluding the contribution of epithelium-derived soluble factors but emphasizing the mandatory role of intercellular contact. The employment of blocking antibodies, however, denied a role for the adhesion molecules intercellular adhesion molecule-1 and vascular cell adhesion molecule-1, or CD11b/CD18 and CD49d/CD29. In essence, infection of alveolar epithelial cells with M. catarrhalis might amplify the inflammatory capacity of invading monocytes eliciting their superoxide production. The epithelial response to this microbial challenge thus clearly differed from that to proinflammatory cytokines. 
