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Infant formula alters surfactant protein A (SP-A) and SP-B expression in pulmonary epithelial cells

Maurice G Chen1, Constance L Atkins, Shirley R Bruce

  • 1Division of Neonatal-Perinatal Medicine, Department of Pediatrics, The University of Texas Health Science Center at Houston, Houston, Texas 77030, USA.

Pediatric Pulmonology
|April 27, 2011
PubMed

Insights

Infant formula exposure in lung cells reduces critical surfactant proteins (SP-A and SP-B), potentially impairing lung defense and innate immunity. This effect is dose-dependent and linked to cow milk components.

Area of Science:

  • Pulmonary Medicine
  • Cell Biology
  • Neonatal Health

Background:

  • Pulmonary surfactant proteins A (SP-A) and SP-B are vital for lung function, reducing surface tension and providing innate immunity.
  • Infant formula aspiration can cause lung issues, but its direct impact on surfactant protein expression is unknown.

Purpose of the Study:

  • To investigate the in vitro effects of infant formula on surfactant protein homeostasis in pulmonary epithelial cells.
  • To determine if infant formula alters the gene expression of SP-A and SP-B.

Main Methods:

  • Cultured human (NCI-H441) and mouse (MLE15) pulmonary epithelial cells were exposed to infant formula for 6 hours.
  • Surfactant protein A and B gene and protein expression levels were measured at 18 and 42 hours post-exposure.

Main Results:

  • Infant formula significantly reduced SP-A and SP-B mRNA and SP-A protein in a dose-dependent manner.
  • SP-A mRNA remained suppressed at 42 hours, while SP-B mRNA showed a 10-fold increase.
  • Soy formula and non-fat dry milk did not affect SP-A and SP-B mRNA levels, indicating a role for cow milk-derived components.

Conclusions:

  • Infant formula directly impacts pulmonary surfactant protein gene expression.
  • Milk aspiration may compromise the lung's ability to combat environmental challenges due to altered surfactant protein levels.

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