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Infant formula alters surfactant protein A (SP‐A) and SP‐B expression in pulmonary epithelial cells
Author(s) -
Chen Maurice G.,
Atkins Constance L.,
Bruce Shirley R.,
Khan Amir M.,
Liu Yuying,
Alcorn Joseph L.
Publication year - 2011
Publication title -
pediatric pulmonology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.866
H-Index - 106
eISSN - 1099-0496
pISSN - 8755-6863
DOI - 10.1002/ppul.21455
Subject(s) - pulmonary surfactant , messenger rna , lung , gene expression , in vitro , infant formula , medicine , surfactant protein a , immunology , andrology , endocrinology , microbiology and biotechnology , biology , gene , biochemistry
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. Pediatr. Pulmonol. 2011; 46:903–912. © 2011 Wiley‐Liss, Inc.