OBJECTIVE: To investigate the effect of pulmonary surfactant (PS) on the Th1/Th2 balance and serum levels of interleukin-4 (IL-4), interferon-γ (IFN-γ) and IgE in neonates with respiratory distress syndrome (RDS). METHODS: A total of 58 neonates with RDS were divided into control (n=20) and PS treatment groups (n=38). The control group underwent mechanical ventilation and other conventional treatment, while the PS treatment group received with bovine PS treatment within 1 hour of being admitted to the hospital together with mechanical ventilation and other conventional treatment. Enzyme-linked immunosorbent assay was used to measure serum levels of IL-4, IFN-γ and IgE before treatment and 24, 48 and 72 hours after treatment. Simultaneously, arterial blood gas, respiratory system compliance, and other ventilator parameters were recorded. RESULTS: Compared with the control group, the PS treatment group showed significantly shorter duration of mechanical ventilation and oxygen exposure time (P<0.05), significantly better respiratory system compliance and significantly lower oxygenation index 24, 48 and 72 hours after treatment (P<0.05). At 48 and 72 hours after treatment, serum levels of IFN-γ were significantly lower in the PS treatment group than in the control group (120±46 ng/L vs 229±59 ng/L, P<0.05; 141±40 ng/L vs 282±44 ng/L, P<0.05), and serum levels of IL-4 were significantly higher in the PS treatment group than in the control group (263±48 pg/mL vs 152±45 pg/mL, P<0.05; 417±49 pg/mL vs 201±46 pg/mL, P<0.05). At 72 hours after treatment, serum level of IgE was significantly lower in the PS treatment group than in the control group (115±44 pg/mL vs 199±43 ng/mL; P<0.05). CONCLUSIONS: PS treatment can shorten the duration of mechanical ventilation and oxygen exposure time, regulate serum levels of IFN-γ, IL-4 and IgE, and influence Th1/Th2 balance in neonates with RDS, thus inhibiting lung inflammatory response and reducing lung injury.
Key words
Respiratory distress syndrome /
Pulmonary surfactant /
Th1/Th2 balance /
Interleukin-4 /
Interferon-γ /
IgE /
Neonate
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References
[1]Kamath BD, Macguire ER, McClure EM, Goldenberg RL, Jobe AH. Neonatal mortality from respiratory distress syndrome: lessons for low-resource countries[J]. Pediatrics, 2011, 127(6): 1139-1146.
[2]Sweet D, Bevilacqua G, Carnielli V, Greisen G, Plavka R, Saugstad OD, et al. European consensus guidelines on the management of neonatal respiratory distress syndrome[J]. J Perinat Med, 2007, 35(3): 175-186.
[3]Speer CP. Neonatal respiratory distress syndrome: an inflammatory disease?[J]. Neonatology, 2011, 99(4): 316-319.
[4]康妍萌,丁明杰,韩玉玲,王世富,马香,李华. 重症肺炎支原体肺炎患儿肺泡灌洗液中 Th1/Th2 细胞免疫应答状况的研究 [J].中国当代儿科杂志, 2011, 13(3): 188-190.
[5]Kellner J, Gamarra F, Welsch U, Jorres RA, Huber RM, Bergner A. IL-13Rα2 reverses the effects of IL-13 and IL-4 on bronchial reactivity and acetylcholine-induced Ca2+ signalling[J]. Int Arch Allergy Immunol, 2007, 142(3): 199-210.
[6]史瑞明,雷春莲,包瑛,罗树舫. 肺炎支原体下呼吸道感染患儿外周血Th细胞亚群Th1/Th2及B细胞研究[J]. 西安交通大学学报:医学版,2003,24(3):234-236.
[7]邵晓梅, 叶鸿瑁, 丘小汕. 实用新生儿学[M]. 第四版. 北京:人民卫生出版社,2004:421-427.
[8]Sweet DG, Carnielli V, Greisen G, Hallman M, Ozek E, Plavka R, et al. "European consensus guidelines on the management of neonatal respiratory distress syndrome in preterm infants-2010 update"[J]. Neonatology, 97(4): 402-417.
[9]黄波, 罗小平. 宫内炎性因子暴露与胎肺发育[J].中华围产医学杂志,2005, 8(6):426-429.
[10]Jobe AH, Ikegami M. Antenatal infection/inflammation and postnatal lung maturation and injury[J]. Respir Res, 2001, 2(1): 27-32.
[11]Speer CP. Chorioamnionitis, postnatal factors and proinflammatory response in the pathogenetic sequence of bronchopulmonary dysplasia [J]. Neonatology, 2009, 95(4): 353-361.
[12]刘云, 李丽, 梁文英, 聂春霞. 不同种类肺表面活性物质治疗新生儿呼吸窘迫综合征的疗效比较[J]. 中国当代儿科杂志,2012,14(4):253-255.
[13]马靖. Th1/Th2反应与人类肺部疾病[J].国外医学呼吸系统分册. 2000, 20(2):67-69.
[14]Mulligan MS, Warner RL, Foreback JL, Shanley TP, Ward PA. Protective effects of IL-4, IL-10, IL-12,and IL-13 in IgG immune complex-induced lung injury: role of endogenous IL-12[J]. J Immunol, 1997,159(7):3483-3489.
[15]Vecchiarelli A, Siracusa A, Monari C, Pietrella D, Retini C, Severini C. Cytokine regulation of low affinity IgE receptor (CD23) on monocytes from asthmatic subjects[J]. Clin Exp Immunol, 1994, 97(2):248-251.
[16]Berger A. Th1 and Th2 responses: What are they?[J]. BMJ, 2000, 321(7258): 424.
[17]Tanaka T, Hu-Li J, Seder RA, Fazekas de St Groth B, Paul WE. Interleukin 4 suppresses interleukin 2 and interferon gamma production by naive T cells stimulated by accessory cell-dependent receptor engagement[J]. Proc Natl Sci U S A, 1993, 90(13): 5914-5918.
[18]Koch L, Fritzsching B, Frommhold D, Poeschl J. Lipopolysaccharide-induced expression of Th1/Th2 cytokines in whole neonatal cord and adult blood: role of nuclear factorkappa B and p38 MAPK [J]. Neonatology, 2011, 99(2): 140-145.
[19]常立文,李文斌. 新生儿急性肺损伤/急性呼吸窘迫综合征 [J]. 实用儿科临床杂志,2007,22(2):85-87.
[20]阳艳丽, 潘玉琴, 何帮顺, 钟天鹰. 哮喘患儿外周血调节性 T 细胞和 Th1/Th2 的变化及其与哮喘病情的关系[J]. 中国当代儿科杂志,2011, 13(6):482-486.
[21]支涤静,王晓川,沈水仙,罗飞宏,苏贻新,方昕. 儿童1型糖尿病Th1/Th2免疫应答状态研究[J]. 中华儿科杂志, 2001,39(3):148-150.