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Published ahead of print on January 24, 2005, doi:10.1165/rcmb.2004-0309OC

Am. J. Respir. Cell Mol. Biol., Volume 32, Number 4, April 2005, 311-318

A more recent version of this article appeared on April 1, 2005
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Submitted on September 29, 2004
Revised on January 21, 2005

IL-1{beta} causes pulmonary inflammation, emphysema, and airway remodeling in the adult murine lung

Urpo Lappalainen1, Jeffrey A Whitsett2, Susan E Wert2, Jay W Tichelaar3, and Kristina Bry1*

1 Department of Pediatrics, Goteborg University, Goteborg, Sweden, 2 Divisions of Neonatology and Pulmonary Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA, 3 Department of Environmental Health, University of Cincinnati, Cincinnati, OH, USA

* To whom correspondence should be addressed. E-mail: kristina.bry{at}pediat.gu.se.

The production of the inflammatory cytokine IL-1 is increased in lungs of patients with chronic obstructive pulmonary disease (COPD) or asthma. In order to characterize the in vivo actions of IL-1 in the lung, transgenic mice were generated in which human IL-1{beta} was expressed in the lung epithelium with a doxycycline-inducible system controlled by the rat Clara cell secretory protein (CCSP) promoter. Induction of IL-1{beta} expression in the lungs of adult mice caused pulmonary inflammation characterized by neutrophil and macrophage infiltrates. IL-1{beta} caused distal airspace enlargement, consistent with emphysema. IL-1{beta} caused disruption of elastin fibers in alveolar septa and fibrosis in airway walls and in the pleura. IL-1{beta} increased the thickness of conducting airways, enhanced mucin production, and caused lymphocytic aggregates in the airways. Decreased immunostaining for the winged helix transcription factor FOXA2 was associated with goblet cell hyperplasia in IL-1{beta}-expressing mice. The production of the neutrophil-attractant CXC chemokines, KC (CXCL1) and MIP-2 (CXCL2), and of matrix metalloproteases, MMP-9 and MMP-12, was increased by IL-1{beta}. Chronic production of IL-1{beta} in respiratory epithelial cells of adult mice causes lung inflammation, enlargement of distal airspaces, mucus metaplasia, and airway fibrosis in the adult mouse.




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