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Am J Physiol Lung Cell Mol Physiol 292: L550-L558, 2007. First published October 27, 2006; doi:10.1152/ajplung.00329.2006
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FGF-10 is decreased in bronchopulmonary dysplasia and suppressed by Toll-like receptor activation

John T. Benjamin,1 Rebekah J. Smith,1 Brian A. Halloran,1 Timothy J. Day,4 David R. Kelly,4 and Lawrence S. Prince1,2,3

Departments of 1Pediatrics, 2Physiology and Biophysics, 3Cell Biology, and 4Pathology and Laboratory Medicine, Children's Hospital of Alabama, University of Alabama at Birmingham, Birmingham, Alabama

Submitted 25 August 2006 ; accepted in final form 24 October 2006

Many extremely preterm infants continue to suffer from bronchopulmonary dysplasia, which results from abnormal saccular-stage lung development. Here, we show that fibroblast growth factor-10 (FGF-10) is required for saccular lung development and reduced in the lung tissue of infants with bronchopulmonary dysplasia. Although exposure to bacteria increases the risk of bronchopulmonary dysplasia, no molecular target has been identified connecting inflammatory stimuli and abnormal lung development. In an experimental mouse model of saccular lung development, activation of Toll-like receptor 2 (TLR2) or Toll-like receptor 4 (TLR4) inhibited FGF-10 expression, leading to abnormal saccular airway morphogenesis. In addition, Toll-mediated FGF-10 inhibition disrupted the normal positioning of myofibroblasts around saccular airways, similar to the mislocalization of myofibroblasts seen in patients with bronchopulmonary dysplasia. Reduced FGF-10 expression may therefore link the innate immune system and impaired lung development in bronchopulmonary dysplasia.

innate immunity; lung development; branching morphogensis


Address for reprint requests and other correspondence: Lawrence S. Prince, Dept. of Pediatrics, Division of Neonatology, Univ. of Alabama at Birmingham, VH648C, 1670 Univ. Boulevard, Birmingham, AL 35294 (e-mail: lprince{at}peds.uab.edu)




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