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目的 应用分子生物学技术探讨慢性肺疾病 (CLD)和呼吸窘迫综合征 (RDS)患儿肺部的炎症反应机制。方法 应用原位基因杂交技术 (insitu hybridzation) ,结合免疫组织化学染色技术和常规组织染色技术检测尸解肺组织的炎性细胞浸润和细胞因子基因表达情况 ,结果用中位数 (M)表示。结果 新生儿RDS患儿肺内IL 8mRNA基因表达为 2 7/ 5mm2 ,明显高于对照组的 2 / 5mm2 ,差异有显著性 (U =3 2 3,P <0 0 1) ;CLD患儿肺内IL 8mRNA基因表达为 5 6 / 5mm2 ,也明显高于对照组的4 / 5mm2 ,差异有显著性 (U =5 7 3,P <0 0 1)。RDS组肺间质CD68阳性巨噬细胞 (14 5 / 5mm2 )、白细胞弹性蛋白酶 (N elastase)阳性多核粒细胞 (133/ 5mm2 )均明显高于对照组 (CD68细胞 18/ 5mm2 ,N elastase细胞 2 8/ 5mm2 )。CLD组肺间质CD68阳性巨噬细胞 (中位数为 15 3/ 5mm2 )、N elastase阳性的多核粒细胞 (182 / 5mm2 )均明显高于对照组 (CD68细胞 31/ 5mm2 ,N elastase细胞 37/ 5mm2 )。CD+ 3 淋巴细胞在RDS新生儿肺组织增加不明显 (2 1/ 5mm2 和 17/ 5mm2 ,P >0 0 5 ) ,而在CLD组肺组织中明显高于对照组 (41/ 5mm2 和 5 / 5mm2 ,P <0 0 1)。结论 RDS和CLD可引起肺组织细胞因子基因表达增加 ,提示炎症反应参与了RDS和CLD的病理
Objective To investigate the mechanism of inflammation in the lungs of children with chronic lung disease (CLD) and respiratory distress syndrome (RDS) using molecular biology techniques. Methods The inflammatory cell infiltration and cytokine gene expression in autologous lung tissue were detected by using in situ hybridzation, immunohistochemical staining and routine histological staining. The median (M) values were used for the results. Results The expression of IL-8mRNA in the lungs of neonatal RDS children was 27 / 5mm2, which was significantly higher than that of the control group (2 / 5mm2, U332, P <0.01) The expression of IL-8mRNA was 56 / 5mm2, which was also significantly higher than that of the control group (4 / 5mm2). The difference was significant (U = 573, P <0.01). In RDS group, the expression of interstitial CD68 positive macrophages (14 5 / 5mm2) and Nlastase positive multinucleated granulocytes (133/5 mm2) were significantly higher than that of the control group (CD68 cells 18/5 mm2, Nlastase 2 8 / 5mm2). CD68 positive macrophages (median 15 3/5 mm 2) and Nlastase positive multinucleated granulocytes (182/5 mm 2) in the CLD group were significantly higher than those in the control group (31/5 mm 2 in CD68 cells and 37 in Nlastase cells / 5mm2). CD + 3 lymphocytes in the lung of RDS neonatal lung tissue was not significantly increased (2 1 / 5mm2 and 17 / 5mm2, P> 0 05), while in the CLD group was significantly higher than the control group (41 / 5mm2 and 5 / 5mm2 , P <0 0 1). Conclusions RDS and CLD can cause the increase of cytokine gene expression in lung tissue, suggesting that inflammation is involved in the pathology of RDS and CLD