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Published ahead of print on January 13, 2006, doi:10.1165/rcmb.2005-0436SF
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American Journal of Respiratory Cell and Molecular Biology. Vol. 34, pp. 527-536, 2006
© 2006 American Thoracic Society
DOI: 10.1165/rcmb.2005-0436SF


Airway Epithelium, Inflammation, and Mechanisms of Disease: A Tribute to Carol B. Basbaum

Airway Mucus

From Production to Secretion

Olatunji W. Williams, Amir Sharafkhaneh, Victor Kim, Burton F. Dickey and Christopher M. Evans

Department of Pediatric Medicine and Department of Medicine, Baylor College of Medicine; Michael E. Debakey Houston VA Medical Center; University of Texas M. D. Anderson Cancer Center, Houston, Texas; and Division of Pulmonary and Critical Care Medicine, Temple Lung Center, Temple University Hospital, Philadelphia, Pennsylvania

Correspondence and requests for reprints should be addressed to Christopher M. Evans, Ph.D., Assistant Professor, Department of Pulmonary Medicine, M. D. Anderson Cancer Center, Institute of Biosciences and Technology, 2121 West Holcombe Boulevard, Room 704, Houston, TX 77030. E-mail: cevans{at}mdanderson.org

Abstract

Mucus hypersecretion is a phenotype associated with multiple obstructive lung diseases. However, in spite of its nefarious reputation under pathologic conditions, there are significant benefits to having low levels of mucus present in the airways at baseline, such as the ability to trap and eliminate inhaled particles and to prevent desiccation of airway surfaces. Mucins are high–molecular-weight glycoproteins that are the chief components that render viscoelastic and gel-forming properties to mucus. Recent advances in animal models and in vitro systems have provided a wealth of information regarding the identification of the mucin genes that are expressed in the lungs, the signal transduction pathways that regulate the expression of these mucins, and the secretory pathways that mediate their release into the airways. In addition, the clinical and pathologic literature has corroborated many of the basic laboratory findings. As a result, mucin overproduction and hypersecretion are moving away from being markers of disease and toward being testable as functional components of lung disease processes.

Key Words: epithelium • lung • metaplasia • mucin • secretion




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