Cytokine and chemokine responses in pediatric patients with severe pneumonia associated with pandemic A/H1N1/2009 influenza virus

Cytokine and chemokine responses in pediatric patients with severe pneumonia associated with pandemic A/H1N1/2009 influenza virus
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DOI:
10.1111/j.1348-0421.2012.00489.x
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发表时间:
2012-09-01
影响因子:
2.6
通讯作者:
Yoshikawa, Tetsushi
Yoshikawa, Tetsushi
中科院分区:
医学4区
文献类型:
--
作者:
Matsumoto, Yuji;Kawamura, Yoshiki;Yoshikawa, Tetsushi

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严重肺炎和白细胞增多是甲型h1n1流感病毒感染儿童患者的特征性临床表现,经常观察到。本研究的目的是阐明细胞因子和趋化因子在甲型h1n1流感病毒感染患者并发肺炎和白细胞增多症中的作用。本研究纳入了47例甲型h1n1流感大流行病毒感染患者。肺炎患者白细胞介素-10 (IL -10, P = 0.027)和IL-5 (IL -5, P = 0.014)表达明显高于非肺炎患者。此外,血清中干扰素-?合并中性粒细胞增多的肺炎患者血清IL-4 (P = 0.024)、IL-2 (P = 0.012)、肿瘤坏死因子-a (P = 0.01)、白细胞介素-4 (P = 0.09)水平均显著低于未合并中性粒细胞增多的肺炎患者。在评估的五种血清趋化因子浓度中,只有IL-8在嗜中性粒细胞增多的肺炎患者中显著低于无白细胞增多的肺炎患者(P = 0.001)。这些细胞因子和趋化因子可能在与甲型H1N1/2009流感病毒感染相关的儿童肺炎发病机制中发挥重要作用。
Severe pneumonia and leukocytosis are characteristic, frequently observed, clinical findings in pediatric patients with pandemic A/H1N1/2009 influenza virus infection. The aim of this study was to elucidate the role of cytokines and chemokines in complicating pneumonia and leukocytosis in patients with pandemic A/H1N1/2009 influenza virus infection. Forty-seven patients with pandemic A/H1N1/2009 influenza virus infection were enrolled in this study. Expression of interleukin (IL)-10 (P = 0.027) and IL-5 (P = 0.014) was significantly greater in patients with pneumonia than in those without pneumonia. Additionally, serum concentrations of interferon-? (P = 0.009), tumor necrosis factor-a (P = 0.01), IL-4 (P = 0.024), and IL-2 (P = 0.012) were significantly lower in pneumonia patients with neutrophilic leukocytosis than in those without neutrophilic leukocytosis. Of the five serum chemokine concentrations assessed, only IL-8 was significantly lower in pneumonia patients with neutrophilic leukocytosis than in those without leukocytosis (P = 0.001). These cytokines and chemokines may play important roles in the pathogenesis of childhood pneumonia associated with A/H1N1/2009 influenza virus infection.