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Bronchopulmonary innervation defects in infants and rats with congenital diaphragmatic hernia

Federica Pederiva1, Rosa Aras Lopez, Jose I Rodriguez

  • 1Department of Pediatric Surgery and Research Laboratory, Hospital Universitario La Paz, 28046 Madrid, Spain.

Journal of Pediatric Surgery
|February 16, 2010
PubMed

Insights

Congenital diaphragmatic hernia (CDH) in infants and rats shows reduced nerve trunks but increased glial cells. This altered bronchopulmonary innervation may contribute to respiratory issues in CDH survivors.

Area of Science:

  • Pulmonary Medicine
  • Developmental Biology
  • Neuroscience

Background:

  • Pulmonary morbidity in congenital diaphragmatic hernia (CDH) survivors is a significant clinical challenge.
  • Previous studies indicated deficient tracheal innervation in CDH rat models.
  • The current study investigates abnormalities in bronchopulmonary innervation in both human infants and rat models with CDH.

Purpose of the Study:

  • To examine the innervation of the bronchopulmonary system in congenital diaphragmatic hernia.
  • To compare neural and glial cell distribution in the lungs of CDH and control subjects.
  • To investigate the role of glial cell-derived neurotrophic factor (GDNF) in CDH-associated innervation changes.

Main Methods:

  • Immunohistochemistry was employed on lung tissues from fetal rats (E15, E18, E21) and human infants (CDH and controls).
  • Antibodies targeting Protein gene product 9.5, S100, Neurofilament, and Rearranged during transfection (RET) were used.
  • Quantification of nerve trunks, glial cells, RET-positive cells, and measurement of GDNF protein and mRNA were performed.

Main Results:

  • A decrease in nerve trunks and bronchi was observed in both CDH infants and rat fetuses.
  • An increase in glial cells and RET-positive cells per bronchial surface area was found in CDH subjects.
  • GDNF protein levels were elevated, while GDNF mRNA levels were decreased in preterm CDH rat lungs.

Conclusions:

  • Infants and rats with CDH exhibit reduced bronchopulmonary nerve components, with compensatory increases in supporting glial cells.
  • Persistent high expression of RET and GDNF protein suggests a complex regulatory response.
  • These innervation deficits are hypothesized to contribute to the respiratory morbidity seen in congenital diaphragmatic hernia.
Abstract

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