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The effects of low-moderate dose prenatal ethanol exposure on the fetal and postnatal rat lung

Published online by Cambridge University Press:  08 July 2013

M. E. Probyn ,
J. S. M. Cuffe ,
S. Zanini  and
K. M. Moritz
M. E. Probyn
Affiliation:
School of Biomedical Sciences, Faculty of Science, The University of Queensland, St Lucia, Australia
J. S. M. Cuffe
Affiliation:
School of Biomedical Sciences, Faculty of Science, The University of Queensland, St Lucia, Australia
S. Zanini
Affiliation:
School of Biomedical Sciences, Faculty of Science, The University of Queensland, St Lucia, Australia
K. M. Moritz*
Affiliation:
School of Biomedical Sciences, Faculty of Science, The University of Queensland, St Lucia, Australia
*
*Address for correspondence: K. M. Moritz, School of Biomedical Sciences, University of Queensland, St Lucia 4067, Australia. Email k.moritz@uq.edu.au
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Abstract

Little is known about whether exposure of the fetus to alcohol alters pulmonary development or function. This study aimed to determine whether low-moderate ethanol (EtOH) exposure throughout gestation alters structural and non-respiratory functional aspects of the fetal and postnatal lung. Sprague–Dawley rats were fed an ad libitum liquid diet ±6% v/v EtOH daily throughout pregnancy, achieving a plasma ethanol (EtOH) concentration of 0.03%. Gene and protein expression was determined in pulmonary tissue collected from fetuses at embryonic day (E) 20 and adult offspring. The percentage of airspace and alveolar size was measured in pulmonary tissue collected at postnatal day (PN) 1. At E20, EtOH-exposed fetuses had decreased aquaporin 5 mRNA levels and a non-significant trend for decreased epithelial sodium channel type α; expression of other pulmonary fluid homeostatic and development genes and surfactant protein genes were not different between groups. At PN1, there was no difference between EtOH-exposed and control offspring in the distal airspace percentage or diameter. At 8 months, collagen type III α1 gene expression was upregulated in EtOH-exposed male offspring; this was associated with increased collagen deposition at 10 months. At 19 months, male EtOH-exposed offspring had a 25% reduction in the protein levels of surfactant protein B. The alterations observed in male EtOH-exposed offspring suggest chronic low-moderate prenatal EtOH-exposure during development may result in increased pulmonary fibrosis. Such an alteration would decrease the respiratory capacity of the lung.

Keywords

collagen, lung, prenatal alcohol exposure, surfactant protein
Type
Original Article
Information
Journal of Developmental Origins of Health and Disease , Volume 4 , Issue 5 , October 2013 , pp. 358 - 367
Copyright
Copyright © Cambridge University Press and the International Society for Developmental Origins of Health and Disease 2013 

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References

1.Harding, R, Hooper, SB. Regulation of lung expansion and lung growth before birth. J Appl Physiol. 1996; 81, 209–224.Google Scholar
2.Maritz, GS, Cock, ML, Louey, S, et al. Effects of fetal growth restriction on lung development before and after birth: a morphometric analysis. Pediatr Pulmonol. 2001; 32, 201–210.CrossRefGoogle ScholarPubMed
3.Maritz, GS, Cock, ML, Louey, S, Suzuki, K, Harding, R. Fetal growth restriction has long-term effects on postnatal lung structure in sheep. Pediatr Res. 2004; 55, 287–295.Google Scholar
4.Maritz, GS, Morley, CJ, Harding, R. Early developmental origins of impaired lung structure and function. Early Hum Dev. 2005; 81, 763–771.Google Scholar
5.Nikolajev, K, Heinonen, K, Hakulinen, A, Lansimies, E. Effects of intrauterine growth retardation and prematurity on spirometric flow values and lung volumes at school age in twin pairs. Pediatr Pulmonol. 1998; 25, 367–370.Google Scholar
6.Lopuhaa, CE, Roseboom, TJ, Osmond, C, et al. Atopy, lung function, and obstructive airways disease after prenatal exposure to famine. Thorax. 2000; 55, 555–561.Google Scholar
7.de Sanctis, L, Memo, L, Pichini, S, Tarani, L, Vagnarelli, F. Fetal alcohol syndrome: new perspectives for an ancient and underestimated problem. J Matern Fetal Neonatal Med. 2011; 24(Suppl 1), 34–37.CrossRefGoogle ScholarPubMed
8.Giglia, RC, Binns, CW. Alcohol, pregnancy and breastfeeding; a comparison of the 1995 and 2001 National Health Survey data. Breastfeed Rev. 2008; 16, 17–24.Google Scholar
9.Zervoudakis, IA, Krauss, A, Fuchs, F. Infants of mothers treated with ethanol for premature labor. Am J Obstet Gynecol. 1980; 137, 713–718.Google Scholar
10.Gauthier, TW, Ping, XD, Gabelaia, L, Brown, LA. Delayed neonatal lung macrophage differentiation in a mouse model of in utero ethanol exposure. Am J Physiol Lung Cell Mol Physiol. 2010; 299, L8–L16.Google Scholar
11.Ping, XD, Harris, FL, Brown, LA, Gauthier, TW. In vivo dysfunction of the term alveolar macrophage after in utero ethanol exposure. Alcohol Clin Exp Res. 2007; 31, 308–316.Google Scholar
12.Gauthier, TW, Young, PA, Gabelaia, L, et al. In utero ethanol exposure impairs defenses against experimental group B streptococcus in the term guinea pig lung. Alcohol Clin Exp Res. 2009; 33, 300–306.Google Scholar
13.Inselman, LS, Fisher, SE, Spencer, H, Atkinson, M. Effect of intrauterine ethanol exposure on fetal lung growth. Pediatr Res. 1985; 19, 12–14.Google Scholar
14.Wang, X, Gomutputra, P, Wolgemuth, DJ, Baxi, L. Effects of acute alcohol intoxication in the second trimester of pregnancy on development of the murine fetal lung. Am J Obstet Gynecol. 2007; 197, 269, e261–e264.Google Scholar
15.Sozo, F, O'Day, L, Maritz, G, et al. Repeated ethanol exposure during late gestation alters the maturation and innate immune status of the ovine fetal lung. Am J Physiol Lung Cell Mol Physiol. 2009; 296, L510–L518.Google Scholar
16.Probyn, ME, Zanini, S, Ward, LC, Bertram, JF, Moritz, KM. A rodent model of low- to moderate-dose ethanol consumption during pregnancy: patterns of ethanol consumption and effects on fetal and offspring growth. Reprod Fertil Dev. 2012; 24, 859–870.Google Scholar
17.Scherle, W. A simple method for volumetry of organs in quantitative stereology. Mikroskopie. 1970; 26, 57–60.Google Scholar
18.Singh, RR, Cullen-McEwen, LA, Kett, MM, et al. Prenatal corticosterone exposure results in altered AT1/AT2, nephron deficit and hypertension in the rat offspring. J Physiol. 2007; 579, 503–513.CrossRefGoogle ScholarPubMed
19.Weibel, ER. Morphometry of the Human Lung, 1963. Springer-Verlag: Berlin.Google Scholar
20.Le Saux, O, Teeters, K, Miyasato, S, et al. The role of caveolin-1 in pulmonary matrix remodeling and mechanical properties. Am J Physiol Lung Cell Mol Physiol. 2008; 295, L1007–L1017.Google Scholar
21.Guidot, DM, Modelska, K, Lois, M, et al. Ethanol ingestion via glutathione depletion impairs alveolar epithelial barrier function in rats. Am J Physiol Lung Cell Mol Physiol. 2000; 279, L127–L135.Google Scholar
22.Holguin, F, Moss, I, Brown, LA, Guidot, DM. Chronic ethanol ingestion impairs alveolar type II cell glutathione homeostasis and function and predisposes to endotoxin-mediated acute edematous lung injury in rats. J Clin Invest. 1998; 101, 761–768.Google Scholar
23.Flecknoe, SJ, Wallace, MJ, Cock, ML, Harding, R, Hooper, SB. Changes in alveolar epithelial cell proportions during fetal and postnatal development in sheep. Am J Physiol Lung Cell Mol Physiol. 2003; 285, L664–L670.Google Scholar
24.Yamada, T, Suzuki, E, Gejyo, F, Ushiki, T. Developmental changes in the structure of the rat fetal lung, with special reference to the airway smooth muscle and vasculature. Arch Histol Cytol. 2002; 65, 55–69.Google Scholar
25.Volpe, MV, Martin, A, Vosatka, RJ, Mazzoni, CL, Nielsen, HC. Hoxb-5 expression in the developing mouse lung suggests a role in branching morphogenesis and epithelial cell fate. Histochem Cell Biol. 1997; 108, 495–504.Google Scholar
26.Meyer, KC. Aging. Proc Am Thorac Soc. 2005; 2, 433–439.Google Scholar
27.Lucas, JS, Inskip, HM, Godfrey, KM, et al. Small size at birth and greater postnatal weight gain: relationships to diminished infant lung function. Am J Respir Crit Care Med. 2004; 170, 534–540.CrossRefGoogle ScholarPubMed
28.Maritz, GS, Harding, R. Life-long programming implications of exposure to tobacco smoking and nicotine before and soon after birth: evidence for altered lung development. Int J Environ Res Public Health. 2011; 8, 875–898.Google Scholar
29.Moss, M, Bucher, B, Moore, FA, Moore, EE, Parsons, PE. The role of chronic alcohol abuse in the development of acute respiratory distress syndrome in adults. JAMA. 1996; 275, 50–54.Google Scholar
30.Sozo, F, Vela, M, Stokes, V, et al. Effects of prenatal ethanol exposure on the lungs of postnatal lambs. Am J Physiol Lung Cell Mol Physiol. 2011; 300, L139–L147.Google Scholar
31.Katzenstein, AL. Smoking-related interstitial fibrosis (SRIF), pathogenesis and treatment of usual interstitial pneumonia (UIP), and transbronchial biopsy in UIP. Mod Pathol. 2012; 25(Suppl 1), S68–S78.Google Scholar
32.Greene, KE, Wright, JR, Steinberg, KP, et al. Serial changes in surfactant-associated proteins in lung and serum before and after onset of ARDS. Am J Respir Crit Care Med. 1999; 160, 1843–1850.Google Scholar
33.Gregory, TJ, Longmore, WJ, Moxley, MA, et al. Surfactant chemical composition and biophysical activity in acute respiratory distress syndrome. J Clin Invest. 1991; 88, 1976–1981.Google Scholar
34.Melton, KR, Nesslein, LL, Ikegami, M, et al. SP-B deficiency causes respiratory failure in adult mice. Am J Physiol Lung Cell Mol Physiol. 2003; 285, L543–L549.Google Scholar
35.Griese, M. Pulmonary surfactant in health and human lung diseases: state of the art. Eur Respir J. 1999; 13, 1455–1476.CrossRefGoogle ScholarPubMed
36.Probyn, ME, Parsonson, KR, Gardebjer, EM, et al. Impact of low dose prenatal ethanol exposure on glucose homeostasis in Sprague–Dawley rats aged up to eight months. PLoS One. 2013; 8, e59718.Google Scholar
37.Cullen, CL, Burne, TH, Lavidis, NA, Moritz, KM. Low dose prenatal ethanol exposure induces anxiety-like behaviour and alters dendritic morphology in the basolateral amygdala of rat offspring. PLoS One. 2013; 8, e54924.CrossRefGoogle ScholarPubMed
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