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This Article Full Text Full Text (PDF) All Versions of this Article: 296/3/L510    most recent 90532.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Sozo, F. Articles by Harding, R. Search for Related Content PubMed PubMed Citation Articles by Sozo, F. Articles by Harding, R.

Repeated ethanol exposure during late gestation alters the maturation and innate immune status of the ovine fetal lung

¹Department of Anatomy and Developmental Biology, Monash University, Melbourne, Victoria, Australia; ²Department of Medical Biosciences, University of the Western Cape, Bellville, South Africa; ³Department of Physiology, Monash University, Melbourne, Victoria, Australia; ⁴Department of Obstetrics and Gynaecology, University of Toronto, Toronto, Ontario, Canada; and ⁵Department of Pharmacology and Toxicology, Queen's University, Kingston, Ontario, Canada

Submitted 22 October 2008 ; accepted in final form 19 December 2008

Little is known about the effects of fetal ethanol exposure on lung development. Our aim was to determine the effects of repeated ethanol exposure during late gestation on fetal lung growth, maturation, and inflammatory status. Pregnant ewes were chronically catheterized at 91 days of gestational age (DGA; term 147 days). From 95-133 DGA, ewes were given a 1-h daily infusion of either 0.75 g ethanol/kg (n = 9) or saline (n = 8), with tissue collection at 134 DGA. Fetal lungs were examined for changes in tissue growth, structure, maturation, inflammation, and oxidative stress. Between treatment groups, there were no differences in lung weight, DNA and protein contents, percent proliferating and apoptotic cells, tissue and air-space fractions, alveolar number and mean linear intercept, septal thickness, type-II cell number and elastin content. Ethanol exposure caused a 75% increase in pulmonary collagen I 1 mRNA levels (P < 0.05) and a significant increase in collagen deposition. Surfactant protein (SP)-A and SP-B mRNA levels were approximately one third of control levels following ethanol exposure (P < 0.05). The mRNA levels of the proinflammatory cytokines interleukin (IL)-1β and IL-8 were also lower (P < 0.05) in ethanol-exposed fetuses compared with controls. Pulmonary malondialdehyde levels tended to be increased (P = 0.07) in ethanol-exposed fetuses. Daily exposure of the fetus to ethanol during the last third of gestation alters extracellular matrix deposition and surfactant protein gene expression, which could increase the risk of respiratory distress syndrome after birth. Changes to the innate immune status of the fetus could increase the susceptibility of the neonatal lungs to infection.

lung growth; lung morphometry; surfactant proteins; proinflammatory cytokines