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

Abstract

Surfactant proteins A (SP-A) and SP-B are critical in the ability of pulmonary surfactant to reduce alveolar surface tension and provide innate immunity. Aspiration of infant milk formula can lead to lung dysfunction, but direct effects of aspirated formula on surfactant protein expression in pulmonary cells have not been described. The hypothesis that infant formula alters surfactant protein homeostasis was tested in vitro by assessing surfactant protein gene expression in cultured pulmonary epithelial cell lines expressing SP-A and SP-B that were transiently exposed (6 hr) to infant formula. Steady-state levels of SP-A protein and mRNA and SP-B mRNA in human bronchiolar (NCI-H441) and mouse alveolar (MLE15) epithelial cells were reduced in a dose-dependent manner 18 hr after exposure to infant formula. SP-A mRNA levels remained reduced 42 hr after exposure, but SP-B mRNA levels increased 10-fold. Neither soy formula nor non-fat dry milk affected steady-state SP-A and SP-B mRNA levels; suggesting a role of a component of infant formula derived from cow milk. These results indicate that infant formula has a direct, dose-dependent effect to reduce surfactant protein gene expression. Ultimately, milk aspiration may potentially result in a reduced capacity of the lung to defend against environmental insults.

Oral Administration of Surfactant Protein‐A Reduces Pathology in an Experimental Model of Necrotizing Enterocolitis

“…This includes the intestine, in which differential allele-specific expression of SP-A has been observed (12,13). We previously reported that SP-A expression is reduced in a human bronchiolar cell line (H441) upon transient exposure to infant formula (37). Based on those results and the fact that this model of neonatal NEC requires formula feeding, we postulated that a reduction in intestinal levels of SP-A may play a role in the development of NEC in our experimental rat model.…”

Correlation between surfactant protein B mRNA expression and neonatal respiratory distress syndrome

“…Pulmonary surfactant is crucial in the reduction of the surface tension at the air-water interface where pulmonary surfactant is degraded and recycled. SP-B is an important pulmonary surfactant-associated protein capable of reducing or altering the surface tension by changing the surface area, preventing alveolar collapse ( 1 – 3 ). Studies have shown SP-B protein deficiency to be associated with the pathogenesis of neonatal respiratory distress syndrome (RDS) ( 4 , 5 ).…”