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Published ahead of print on July 18, 2003, doi:10.1165/rcmb.2002-0267OC

Am. J. Respir. Cell Mol. Biol., Volume 30, Number 2, February 2004, 193-201

A more recent version of this article appeared on February 1, 2004
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Submitted on November 22, 2002
Revised on July 15, 2003

Neutrophil defensins enhance lung epithelial wound closure and mucin gene expression in vitro

Jamil Aarbiou1*, Renate M Verhoosel1, Sandra van Wetering1, Willem I de Boer1, J. Han J van Krieken2, Sergey V Litvinov3, Klaus F Rabe1, and Pieter S Hiemstra1

1 Pulmonology, Leiden University Medical Center, Leiden, The Netherlands, 2 Pathology, University Medical Center St. Radboud, Nijmegen, The Netherlands, 3 Pathology, Leiden University Medical Center, Leiden, The Netherlands

* To whom correspondence should be addressed. E-mail: j.aarbiou{at}lumc.nl.

Human airways are frequently exposed to potentially harmful agents that cause tissue injury. Upon such injury, a repair process is initiated that comprises cell migration, proliferation and differentiation. We have previously shown that human neutrophil defensins (HNP1-3) induce airway epithelial cell proliferation. Because of the role of cell proliferation in epithelial wound repair, we investigated the effect of HNP1-3 on airway epithelial wound closure and mucin gene expression in vitro. Using NCI-H292 airway epithelial cell cultures, we demonstrated that HNP1-3 cause a dose- and time-dependent increase of wound closure as well as increased cell migration. Furthermore, HNP1-3 caused a biphasic activation of the MAP kinase ERK1/2. Both the effects of HNP1-3 on wound closure and ERK1/2 activation were blocked by specific inhibitors of the MAP kinase kinase MEK, while inhibitors of epidermal growth factor (EGF) receptor tyrosine kinase, phosphatidylinositol 3-kinase (PI-3K) and Src did block defensin-enhanced wound closure but not ERK1/2 activation. Finally, HNP1-3 increased mRNA encoding the mucins MUC5B and MUC5AC, suggesting a role for defensins in mucous cell differentiation. These results indicate that neutrophil defensins increase epithelial wound repair in vitro, that involves migration and proliferation, and mucin production. Neutrophil defensin-enhanced wound repair appears to require EGF receptor activation and downstream signaling pathways.




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