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
Am J Physiol Lung Cell Mol Physiol. 2007 292 (2): L550-8

PMID: 17071719 · DOI:10.1152/ajplung.00329.2006

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.

MeSH Terms (18)

Animals Bronchopulmonary Dysplasia Disease Models, Animal Female Fetus Fibroblast Growth Factor 10 Fibroblasts Gene Expression Regulation Humans Infant, Newborn Lipopolysaccharides Lung Mice Mice, Inbred BALB C RNA, Messenger Toll-Like Receptor 2 Toll-Like Receptor 4 Transforming Growth Factor beta

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