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    Am J Physiol Lung Cell Mol Physiol. 2007 Feb;292(2):L550-8. Epub 2006 Oct 27.

    FGF-10 is decreased in bronchopulmonary dysplasia and suppressed by Toll-like receptor activation.

    Benjamin JT, Smith RJ, Halloran BA, Day TJ, Kelly DR, Prince LS.

    Source

    Departments of Pediatrics, Children's Hospital of Alabama, University of Alabama at Birmingham, Birmingham, AL 35294, USA.

    Abstract

    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.

    PMID:
    17071719
    [PubMed - indexed for MEDLINE]
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