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Published ahead of print on August 3, 2006, doi:10.1165/rcmb.2006-0116OC

Am. J. Respir. Cell Mol. Biol., Volume 36, Number 1, January 2007, 32-42

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Submitted on March 21, 2006
Revised on August 2, 2006

IL-1{beta} Disrupts Postnatal Lung Morphogenesis in the Mouse

Kristina Bry1*, Jeffrey A Whitsett2, and Urpo Lappalainen1

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

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

Pulmonary inflammation and increased production of the inflammatory cytokine IL-1{beta} are associated with the development of bronchopulmonary dysplasia (BPD) in premature infants. To study the actions of IL-1{beta} in the fetal and newborn lung in vivo, we developed a bitransgenic mouse in which IL-1{beta} is expressed under conditional control in airway epithelial cells. Perinatal pulmonary expression of IL-1{beta} caused respiratory insufficiency that was associated with increased postnatal mortality. While intrauterine growth of IL-1{beta}-expressing mice was normal, their postnatal growth was impaired. IL-1{beta} disrupted alveolar septation and caused abnormalities in {alpha}-smooth muscle actin and elastin deposition in the septa of distal airspaces. IL-1{beta} disturbed capillary development and inhibited the production of VEGF in the lungs of infant mice. IL-1{beta} induced the expression of CXC chemokines KC (CXCL1) and MIP-2 (CXCL2) and of CC chemokines MCP-1 (CCL2) and MCP-3 (CCL7), consistent with neutrophilic and monocytic infiltration of the lungs. IL-1{beta} caused goblet cell metaplasia and bronchial smooth muscle hyperplasia. Perinatal expression of IL-1{beta} in epithelial cells of the lung caused a lung disease that was clinically and histologically similar to BPD.




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