Our aim was to determine whether fetal exposure to intraamniotic lipopolysaccharide (LPS) persistently alters the lungs following moderate preterm birth. Fetal sheep were exposed to LPS (1 mg/d) or saline from 0.75 to preterm birth at 0.90 of gestation. Eleven weeks after preterm birth, lung structure was unaltered. Interleukin (IL)-1beta messenger RNA (mRNA) levels were elevated in lungs of LPS-exposed lambs (P <.05) but IL-1beta protein levels were unaltered. Lung mRNA levels of IL-6, IL-8 and tumor necrosis factor alpha, and percentage of inflammatory cells were not different between groups. Surfactant protein (SP)-A and SP-C mRNA levels and SP-B tissue protein expression were higher in LPS-exposed lambs than controls (all P <.05); however, expression of SP-A and SP-C proteins was reduced. Prenatal LPS exposure causes a persistent increase in gene expression of proinflammatory mediators and surfactant proteins and a decrease in lung tissue SP-A and -C protein expression after preterm birth, which may affect lung immunity.
Atik, A. A., Sozo, F., Orgeig, S., Suri, L., Hanita, T., Harding, R., & De Matteo, R. M. (2012). Long-term pulmonary effects of intrauterine exposure to endotoxin following preterm birth in sheep. Reproductive Sciences, 19(12), 1352 - 1364. https://doi.org/10.1177/1933719112450327