Abstract With the development of treatment, the survival rate of premature infants has significantly increased, especially extremely premature infants and very low birth weight infants. This has led to an increase in incidence of bronchopulmonary dysplasia (BPD) year by year. BPD has been one of the most common respiratory system diseases in premature infants, especially the small premature infants. Arrested alveolar development is an important cause of BPD. Therefore, the mechanism of arrested alveolar development and the intervention measures for promoting alveolar development are the focuses of research on BPD. Selecting the appropriate animal model of BPD is the key to obtaining meaningful results in the basic research on BPD. Based on above, several common methods for establishing an animal model of BPD and the corresponding changes in pathophysiology are summarized and evaluated in order to provide a reference for selecting the appropriate animal model in studies on the pathogenesis, pathophysiology, and prevention and control strategies of BPD.
XIONG Zeng,ZHOU Xia,YUE Shao-Jie. Methods for establishing animal model of bronchopulmonary dysplasia and their evaluation[J]. CJCP, 2017, 19(1): 121-125.
XIONG Zeng,ZHOU Xia,YUE Shao-Jie. Methods for establishing animal model of bronchopulmonary dysplasia and their evaluation[J]. CJCP, 2017, 19(1): 121-125.
Northway WH Jr, Rosan RC, Porter DY. Pulmonary disease following respirator therapy of hyaline-membrane disease. Bronchopulmonary dysplasia[J]. N Engl J Med, 1967, 276(7):357-368.
[3]
Latini G, De Felice C, Giannuzzi R, et al. Survival rate and prevalence of bronchopulmonary dysplasia in extremely low birth weight infants[J]. Early Hum Dev, 2013, 89(Suppl 1):S69-S73.
[4]
Zysman-Colman Z, Tremblay GM, Bandeali S, et al. Bronchopulmonary dysplasia-trends over three decades[J]. Paediatr Child Health, 2013, 18(2):86-90.
[5]
Carraro S, Filippone M, Da Dalt L, et al. Bronchopulmonary dysplasia:the earliest and perhaps the longest lasting obstructive lung disease in humans[J]. Early Hum Dev, 2013, 89(Suppl 3):S3-S5.
[6]
Bhandari A, McGrath-Morrow S. Long-term pulmonary outcomes of patients with bronchopulmonary dysplasia[J]. Semin Perinatol, 2013, 37(2):132-137.
[7]
Filippone M, Bonetto G, Corradi M, et al. Evidence of unexpected oxidative stress in airways of adolescents born very pre-term[J]. Eur Respir J, 2012, 40(5):1253-1259.
[8]
Wang H, Gao X, Liu C, et al. Morbidity and mortality of neonatal respiratory failure in China:surfactant treatment in very immature infants[J]. Pediatrics, 2012, 129(3):e731-e740.
[9]
Yang H, Fu J, Xue X, et al. Epithelial-mesenchymal transitions in bronchopulmonary dysplasia of newborn rats[J]. Pediatr Pulmonol, 2014, 49(11):1112-1123.
[10]
Sun H, Choo-Wing R, Fan J, et al. Small molecular modulation of macrophage migration inhibitory factor in the hyperoxia-induced mouse model of bronchopulmonary dysplasia[J]. Respir Res, 2013, 14:27.
[11]
Warner BB, Stuart LA, Papes RA, et al. Functional and pathological effects of prolonged hyperoxia in neonatal mice[J]. Am J Physiol, 1998, 275(1 Pt 1):L110-L117.
[12]
Wang M, Luo Z, Liu S, et al. Glutamate mediates hyperoxia-induced newborn rat lung injury through N-methyl-D-aspartate receptors[J]. Am J Respir Cell Mol Biol, 2009, 40(3):260-267.
[13]
Buczynski BW, Yee M, Paige Lawrence B, et al. Lung development and the host response to influenza A virus are altered by different doses of neonatal oxygen in mice[J]. Am J Physiol Lung Cell Mol Physiol, 2012, 302(10):L1078-L1087.
[14]
Sherman MP, Evans MJ, Campbell LA. Prevention of pulmonary alveolar macrophage proliferation in newborn rabbits by hyperoxia[J]. J Pediatr, 1988, 112(5):782-786.
[15]
Galambos C, Sims-Lucas S, Abman SH. Histologic evidence of intrapulmonary anastomoses by three-dimensional reconstruction in severe bronchopulmonary dysplasia[J]. Ann Am Thorac Soc, 2013, 10(5):474-481.
[16]
Hadchouel A, Franco-Montoya ML, Delacourt C. Altered lung development in bronchopulmonary dysplasia[J]. Birth Defects Res A Clin Mol Teratol, 2014, 100(3):158-167.
[17]
Nold MF, Mangan NE, Rudloff I, et al. Interleukin-1 receptor antagonist prevents murine bronchopulmonary dysplasia induced by perinatal inflammation and hyperoxia[J]. Proc Natl Acad Sci U S A, 2013, 110(35):14384-14389.
[18]
Wada K, Jobe AH, Ikegami M. Tidal volume effects on surfactant treatment responses with the initiation of ventilation in preterm lambs[J]. J Appl Physiol(1985), 1997, 83(4):1054-1061.
[19]
Hillman NH, Moss TJ, Nitsos I, et al. Moderate tidal volumes and oxygen exposure during initiation of ventilation in preterm fetal sheep[J]. Pediatr Res, 2012, 72(6):593-599.
[20]
Hillman NH, Kallapur SG, Jobe AH. Physiology of transition from intrauterine to extrauterine life[J]. Clin Perinatol, 2012, 39(4):769-783.
Kallapur SG, Presicce P, Senthamaraikannan P, et al. Intra-amniotic IL-1β induces fetal inflammation in rhesus monkeys and alters the regulatory T cell/IL-17 balance[J]. J Immunol, 2013, 191(3):1102-1109.
[25]
Wright CJ, Kirpalani H. Targeting inflammation to prevent bronchopulmonary dysplasia:can new insights be translated into therapies?[J]. Pediatrics, 2011, 128(1):111-126.
[26]
Ambalavanan N, Nicola T, Hagood J, et al. Transforming growth factor-beta signaling mediates hypoxia-induced pulmonary arterial remodeling and inhibition of alveolar development in newborn mouse lung[J]. Am J Physiol Lung Cell Mol Physiol, 2008, 295(1):L86-L95.
[27]
Olave N, Nicola T, Zhang W, et al. Transforming growth factor-β regulates endothelin-1 signaling in the newborn mouse lung during hypoxia exposure[J]. Am J Physiol Lung Cell Mol Physiol, 2012, 302(9):L857-L865.
[28]
Berger J, Bhandari V. Animal models of bronchopulmonary dysplasia. The term mouse models[J]. Am J Physiol Lung Cell Mol Physiol, 2014, 307(12):L936-L947.
[29]
Huo H, Luo Z, Wang M, et al. MicroRNA expression profile in intrauterine hypoxia-induced pulmonary hypoplasia in rats[J]. Exp Ther Med, 2014, 8(3):747-753.
Harding R, Maritz G. Maternal and fetal origins of lung disease in adulthood[J]. Semin Fetal Neonatal Med, 2012, 17(2):67-72.
[32]
Ratner V, Slinko S, Utkina-Sosunova I, et al. Hypoxic stress exacerbates hyperoxia-induced lung injury in a neonatal mouse model of bronchopulmonary dysplasia[J]. Neonatology, 2009, 95(4):299-305.
[33]
Gortner L, Monz D, Mildau C, et al. Bronchopulmonary dysplasia in a double-hit mouse model induced by intrauterine hypoxia and postnatal hyperoxia:closer to clinical features?[J]. Ann Anat, 2013, 195(4):351-358.
[34]
Monz D, Tutdibi E, Mildau C, et al. Human umbilical cord blood mononuclear cells in a double-hit model of bronchopulmonary dysplasia in neonatal mice[J]. PLoS One, 2013, 8(9):e74740.
[35]
Bry K, Whitsett JA, Lappalainen U. IL-1beta disrupts postnatal lung morphogenesis in the mouse[J]. Am J Respir Cell Mol Biol, 2007, 36(1):32-42.
[36]
Hogmalm A, Bäckström E, Bry M, et al. Role of CXC chemokine receptor-2 in a murine model of bronchopulmonary dysplasia[J]. Am J Respir Cell Mol Biol, 47(6):746-758.
[37]
Aghai ZH, Saslow JG, Mody K, et al. IFN-γ and IP-10 in tracheal aspirates from premature infants:relationship with bronchopulmonary dysplasia[J]. Pediatr Pulmonol, 2013, 48(1):8-13.
[38]
Harijith A, Choo-Wing R, Cataltepe S, et al. A role for matrix metalloproteinase 9 in IFNγ-mediated injury in developing lungs:relevance to bronchopulmonary dysplasia[J]. Am J Respir Cell Mol Biol, 2011, 44(5):621-630.
[39]
Sun H, Choo-Wing R, Sureshbabu A, et al. A critical regulatory role for macrophage migration inhibitory factor in hyperoxia-induced injury in the developing murine lung[J]. PLoS One, 2013, 8(4):e60560.
