Lysozyme Secretion by Submucosal Glands Protects the Airway from Bacterial Infection

Submucosal glands are abundant (approximately 1 gland/mm2) secretory structures in the tracheobronchial airways of the human lung. Because submucosal glands express antibacterial proteins, it has been proposed that they contribute to lung defense. However, this concept is challenged by the fact that...

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Published inAmerican journal of respiratory cell and molecular biology Vol. 32; no. 6; pp. 548 - 552
Main Authors Dajani, Rana, Zhang, Yulong, Taft, Peter J, Travis, Sue M, Starner, Timothy D, Olsen, Ansgar, Zabner, Joseph, Welsh, Michael J, Engelhardt, John F
Format Journal Article
LanguageEnglish
Published United States Am Thoracic Soc 01.06.2005
American Thoracic Society
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Summary:Submucosal glands are abundant (approximately 1 gland/mm2) secretory structures in the tracheobronchial airways of the human lung. Because submucosal glands express antibacterial proteins, it has been proposed that they contribute to lung defense. However, this concept is challenged by the fact that mice do not have submucosal glands in their bronchial airways, yet are quite resistant to bacterial lung infection. The contribution of airway submucosal glands to host defense is also debated as a pathophysiologic component of cystic fibrosis lung disease. Here, we asked whether submucosal glands protect airways against bacterial infection. By comparing tracheal xenograft airways with and without glands, we found that the presence of glands enhanced bacterial killing in vivo and by airway secretions in vitro. Moreover, immunodepletion studies suggested that lysozyme is a major antibacterial component secreted by submucosal glands. These studies provide evidence that submucosal glands are a major source of antibacterials critical for maintaining sterile airways.
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Correspondence and requests for reprints should be addressed to John F. Engelhardt, Department of Anatomy and Cell Biology, University of Iowa, Room 1-111 Bowen Science Building, 51 Newton Road, Iowa City, IA 52242-1109. E-mail: john-engelhardt@uiowa.edu
Conflict of Interest Statement: R.D. has no declared conflicts of interest; Y.Z. has no declared conflicts of interest; P.J.T. has no declared conflicts of interest; S.M.T. has no declared conflicts of interest; T.D.S. has no declared conflicts of interest; A.O. has no declared conflicts of interest; J.Z. has no declared conflicts of interest; M.J.W. has no declared conflicts of interest; and J.F.E. has no declared conflicts of interest.
This study was supported by research funding from NIDDK (DK47967 to J.F.E.), NHLBI (HL061234 to M.J.W.), and the Animal Models Core of the Center for Gene Therapy NIDOK P30 DK54759.
ISSN:1044-1549
1535-4989
DOI:10.1165/rcmb.2005-0059OC