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Articles in PresS, published online ahead of print March 15, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00419.2001
Submitted on October 25, 2001
Accepted on March 11, 2002
1 INSERM U506, Villejuif, France, Metropolitan; Cystic Fibrosis Research Laboratory, Stanford University, Stanford, CA, USA; Herzenberg Laboratory, Stanford University, Stanford, CA, USA
2 INSERM U506, Villejuif, France, Metropolitan
* To whom correspondence should be addressed. E-mail: rabin{at}psych.stanford.edu.
Most cystic fibrosis (CF) patients die of lung failure, due to the combined effects of bacterial infection, neutrophil-mediated inflammation and airway obstruction by hyperviscous mucus. To this day, it remains unclear where and how this pathological vicious circle is initiated in vivo. In particular, it has proven difficult to investigate whether inflammatory pathways are dysregulated in CF airways independently of infection. Also, the relative involvement of large (tracheobronchial) vs. small (bronchiolar) airways in CF pathophysiology is still unclear. To help address these issues, we used an in vivo model based on the maturation of human fetal CF and non-CF small airways in severe combined immunodeficiency (SCID) mice. We show that uninfected mature CF small airway grafts, but not matched non-CF controls, undergo time-dependent neutrophil-mediated inflammation, leading to progressive lung tissue destruction. This model of mature human small airways provides the first clear-cut evidence that, in CF, inflammation may arise at least partly from a primary defect in the regulation of neutrophil recruitment, independently of infection.
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