摘要
目的通过研究早产儿慢性肺疾病外周血17个细胞因子的改变,探讨早产儿慢性肺疾病的部分免疫发病机制。方法将26例住院满28d的早产儿分为慢性肺疾病组(14例)和对照组(12例),用multi-plex技术检测外周血中17个细胞因子(IL-1b,IL-2,IL-4,IL-5,IL-6,IL-7,IL-8,IL-10,IL-12,IL-13,IL-17,GM-CSF,IFN-γ,TNF-α,G-CSF,MCP-1,MIP-1b)的表达水平。结果慢性肺疾病组外周血中的17个细胞因子与对照组相比均无统计学差异(P>0.05)。结论早产儿慢性肺疾病发病后期的发病机制主要不是免疫因素造成的。
Objective To explore the immunomechanism of chronic lung disease（CLD） in prema-ture infants by investigating the changes of 17 cytokines.Methods Twenty-six preterm neonates who had been in the NICU for over 28 days were divided into CLD group（n=14） and control group consisting of 12 preterm neonates.Seventeen cytokines,namely interleukin 1b（IL-1b）,IL-2,IL-4,IL-5,IL-6,IL-7,IL-8,IL-10,IL-12,IL-13,IL-17,granulocyte-macrophage col-ony-stimalating factor,interferon-γ,tumour necrosis factor alpha,granulocyte colony-stimulating factor,monocyte chemoattractant protein 1,and macrophage inflammatory protein-1b were de-tected in a single sample of peripheral blood by multi-plex technology（Bio-plex）.Results There were no significant differences in the level of the 17 cytokines between the two groups（P〉0.05）.Conclusion The cytokines examined may not be involved in the later period pathogenesis of CLD.
出处
《南方医科大学学报》
CAS
CSCD
北大核心
2010年第2期331-333,共3页
Journal of Southern Medical University
基金
广东省自然科学基金(7005170)
关键词
细胞因子
慢性肺疾病
早产儿
cytokines
chronic lung disease
preterm neonates
