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Mediators of Inflammation
Volume 2010 (2010), Article ID 824362, 13 pages
Research Article

Distribution of Major Basic Protein on Human Airway following In Vitro Eosinophil Incubation

1Division of Pulmonary and Critical Care Medicine, Department of Medicine and Pediatrics, Mayo Clinic College of Medicine, Rochester, MN 55905, USA
2Department of Physiology & Biomedical Engineering, Mayo Clinic College of Medicine, Rochester, MN 55905, USA

Received 12 May 2009; Revised 6 November 2009; Accepted 2 January 2010

Academic Editor: Eric Morand

Copyright © 2010 Ailing Xue et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Major basic protein (MBP) released from activated eosinophils may influence airway hyperresponsiveness (AHR) by either direct effects on airway myocytes or by an indirect effect. In this study, human bronchi, freshly isolated human eosinophils, or MBP purified from human eosinophil granules were incubated for studying eosinophil infiltration and MBP localization. Eosinophils immediately adhered to intact human airway as well as to cultured human airway myocytes and epithelium. Following incubation 18–24 h, eosinophils migrated into the airway media, including the smooth muscle layer, but had no specific recruitment to airway neurons. Eosinophils released significant amounts of MBP within the airway media, including areas comprising the smooth muscle layer. Most deposits of MBP were focally discrete and restricted by immunologic detection to a maximum volume of 300  about the eosinophil. Native MBP applied exogenously was immediately deposited on the surface of the airway, but required at least 1 h to become detected within the media of the airway wall. Tissue MBP infiltration and deposition increased in a time- and concentration-dependent manner. Taken together, these findings suggest that eosinophil-derived cationic proteins may alter airway hyperresponsiveness (AHR) in vivo by an effect that is not limited to the bronchial epithelium.