Department of Emergency Medicine, College of Medicine, National Cheng Kung University and Hospital, Tainan 70428, Taiwan ; Center of Infectious Disease and Signaling Research, National Cheng Kung University, Tainan 70428, Taiwan.
Center of Infectious Disease and Signaling Research, National Cheng Kung University, Tainan 70428, Taiwan.
Dis Markers. 2014;2014:195453. doi: 10.1155/2014/195453. Epub 2014 Feb 18.
A novel swine-origin influenza A H1N1 virus (S-OIV) caused human infection and acute respiratory illness in 2009, resulting in an influenza pandemic.
This study characterized the immune responses of S-OIV infection in pediatric patients at risk of pulmonary complications.
All enrolled pediatric patients were confirmed virologically for S-OIV infection in 2009-2010, prospectively. Changes in cellular immunophenotypes were analyzed using flow cytometry. Plasma cytokine levels associated with S-OIV infection by pulmonary and without pulmonary complications were measured using cytokine cytometric bead assay kits.
A total of 85 patients with a mean age of 10.3 years were recruited. The level of C-reactive protein (CRP) was high in patients exhibiting pulmonary complications. The percentage of cellular immunophenotypes did not change between patients with and without pulmonary complications. The absolute numbers of peripheral blood mononuclear cells (PBMC), CD3, CD8, and CD16CD56 decreased with acute S-OIV pulmonary complications. Acute influenza infection with pulmonary complications was associated with high plasma concentrations of IL-1β, IL-6, IL-12, and IFN-γ.
Immunophenotype studies have reported variability in immune response to the severity of S-OIV infections. Acute phase cytokine profiles of the 2009 S-OIV infection might have contributed to the pathogenesis of the pulmonary complications.
一种新型的猪源甲型 H1N1 流感病毒（S-OIV）于 2009 年引发人类感染和急性呼吸道疾病，导致流感大流行。
本研究旨在分析 2009-2010 年患有肺部并发症风险的小儿患者感染 S-OIV 后的免疫反应特征。
所有入组的儿科患者均通过病毒学检测证实感染了 S-OIV。采用流式细胞术分析细胞免疫表型的变化。采用细胞因子流式微球检测试剂盒检测与肺部和无肺部并发症的 S-OIV 感染相关的血浆细胞因子水平。
共招募了 85 名平均年龄为 10.3 岁的患者。伴有肺部并发症的患者 C 反应蛋白（CRP）水平较高。有和无肺部并发症的患者之间细胞免疫表型的百分比没有变化。外周血单核细胞（PBMC）、CD3、CD8 和 CD16CD56 的绝对数量随着急性 S-OIV 肺部并发症而减少。伴有肺部并发症的急性流感感染与高血浆浓度的 IL-1β、IL-6、IL-12 和 IFN-γ相关。
免疫表型研究报告了对 S-OIV 感染严重程度的免疫反应存在差异。2009 年 S-OIV 感染的急性期细胞因子谱可能导致了肺部并发症的发病机制。
