Decreased interleukin-18 response in asthmatic children with severe Mycoplasma pneumoniae pneumonia.
Decreased interleukin-18 response in asthmatic children with severe Mycoplasma pneumoniae pneumonia.
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DOI：
10.1016/j.cyto.2011.02.008
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发表时间：
2011-05
期刊：
影响因子：
3.8
通讯作者：
Kim SG
中科院分区：
文献类型：
--
作者：
Chung HL;Shin JY;Ju M;Kim WT;Kim SG
肺炎支原体（M. pneumoniae）是儿童肺炎的常见病原体。本研究的目的是确定哮喘儿童与非哮喘儿童在急性肺炎支原体肺炎期间所选择的细胞因子或趋化因子反应是否有任何差异。纳入了75名6-12岁的肺炎支原体肺炎儿童。将患者分为两组：已知哮喘患儿（N = 40）和非哮喘患儿（N = 35）。采用ELISA法检测入院患者血浆中白细胞介素(IL)-18及部分趋化因子、IL-8、CXCL9、CXCL10及正常t细胞表达和分泌的活化调节（RANTES）水平。我们研究了这些介质与哮喘状态和患者症状严重程度的关系。还研究了20名年龄匹配的非感染对照。肺炎支原体肺炎患者血浆IL-18及趋化因子水平较未感染、年龄匹配的对照组显著升高（P < 0.01）。而哮喘患者IL-18和CXCL10应答明显低于非哮喘患者（P < 0.01, <0.05），肺炎症状加重（P < 0.01）。重症肺炎组IL-18水平明显低于非重症肺炎组（P < 0.05）。我们的研究提示IL-18及其趋化因子在肺炎支原体肺炎的发病过程中起重要作用。这也提示一些哮喘患儿在感染肺炎支原体肺炎时IL-18反应不足，这可能与本组患者观察到的更为严重的肺炎有关。
Mycoplasma pneumoniae (M. pneumoniae) is a common causative agent of pneumonia in children. The aim of this study is to determine whether there is any difference in selected cytokine or chemokines response in asthmatic children compared to non-asthmatic children during acute M. pneumoniae pneumonia. Seventy-five children, 6–12 years of age, admitted with M. pneumoniae pneumonia were enrolled. Two patient groups were defined: the children with known asthma (N = 40) and non-asthmatic children (N = 35). Interleukin (IL)-18 and selected chemokines, IL-8, CXCL9, CXCL10, and regulation upon activation normal T-cell expressed and secreted (RANTES) were measured by means of ELISA in the plasma samples of the patients collected on admission. We investigated the values of these mediators in relation to the asthma status and symptom severity of the patients. Twenty age-matched, non-infected controls were also studied. Plasma levels of IL-18 and the chemokines increased significantly in the patients with M. pneumoniae pneumonia compared to non-infected, age-matched controls (P < 0.01). However, the asthmatic patients showed significantly reduced IL-18 and CXCL10 responses (P < 0.01, <0.05, respectively) and had more severe pneumonia symptoms (P < 0.01) compared to non-asthmatic patients. IL-18 was significantly lower in severe pneumonia group than in non-severe group (P < 0.05). Our study suggests that IL-18 and the chemokines are importantly involved in the pathogenesis of M. pneumoniae pneumonia. It also indicates that some asthmatic children have deficient IL-18 response when affected by M. pneumoniae pneumonia, which might be associated with more severe pneumonia observed in this group of patients.
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