Major and minor group rhinoviruses elicit differential signaling and cytokine responses as a function of receptor-mediated signal transduction.
Major and minor group rhinoviruses elicit differential signaling and cytokine responses as a function of receptor-mediated signal transduction.
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DOI：
10.1371/journal.pone.0093897
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发表时间：
2014
期刊：
影响因子：
3.7
通讯作者：
Hall DJ
中科院分区：
文献类型：
--
作者：
Schuler BA;Schreiber MT;Li L;Mokry M;Kingdon ML;Raugi DN;Smith C;Hameister C;Racaniello VR;Hall DJ
主要组和次要组人类鼻病毒 (HRV) 通过分别与巨噬细胞和上皮细胞上存在的细胞表面分子 ICAM-1 和 LDL-R 结合而进入宿主。尽管上皮细胞是产生性 HRV 感染的主要部位，但先前的研究表明巨噬细胞参与了鼻病毒诱导的哮喘恶化期间发生的细胞因子失调。对暴露于主要组和次要组 HRV 的原代人类巨噬细胞的转录组分析表明，基因表达存在差异。基因表达的变化可追溯到两种鼻病毒血清型 HRV16（主要组）和 HRV1A（次要组）之间初始 HRV 结合时线粒体活性和信号通路激活的差异。在主要组和次要组 HRV 治疗之间观察到激酶（p38、JNK、ERK5）和转录因子（ATF-2、CREB、CEBP-α）磷酸化的差异。信号通路的差异激活导致哮喘相关细胞因子 CCL20、CCL2 和 IL-10 产生的变化。这是基因相似的病毒引起巨噬细胞不同的细胞因子释放、转录因子磷酸化和 MAPK 激活的第一份报告，表明受体的使用是接触鼻病毒后在人类气道中建立炎症微环境的机制。
Major- and minor-group human rhinoviruses (HRV) enter their host by binding to the cell surface molecules ICAM-1 and LDL-R, respectively, which are present on both macrophages and epithelial cells. Although epithelial cells are the primary site of productive HRV infection, previous studies have implicated macrophages in establishing the cytokine dysregulation that occurs during rhinovirus-induced asthma exacerbations. Analysis of the transcriptome of primary human macrophages exposed to major- and minor-group HRV demonstrated differential gene expression. Alterations in gene expression were traced to differential mitochondrial activity and signaling pathway activation between two rhinovirus serotypes, HRV16 (major-group) and HRV1A (minor-group), upon initial HRV binding. Variances in phosphorylation of kinases (p38, JNK, ERK5) and transcription factors (ATF-2, CREB, CEBP-alpha) were observed between the major- and minor-group HRV treatments. Differential activation of signaling pathways led to changes in the production of the asthma-relevant cytokines CCL20, CCL2, and IL-10. This is the first report of genetically similar viruses eliciting dissimilar cytokine release, transcription factor phosphorylation, and MAPK activation from macrophages, suggesting that receptor use is a mechanism for establishing the inflammatory microenvironment in the human airway upon exposure to rhinovirus.
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影响因子：
3.3
作者：
Fu H;Yang G;Wei M;Liu L;Jin L;Lu X;Wang L;Shen L;Zhang J;Lu H;Yao L;Lu Z
通讯作者：
Lu Z
DOI：
10.1183/09031936.00092410
发表时间：
2011-05
期刊：
The European respiratory journal
影响因子：
--
作者：
Bizzintino J;Lee WM;Laing IA;Vang F;Pappas T;Zhang G;Martin AC;Khoo SK;Cox DW;Geelhoed GC;McMinn PC;Goldblatt J;Gern JE;Le Souëf PN
通讯作者：
Le Souëf PN
影响因子：
8
作者：
通讯作者：
--
影响因子：
46.9
作者：
Ji, Hongkai;Jiang, Hui;Ma, Wenxiu;Johnson, David S.;Myers, Richard M.;Wong, Wing H.
通讯作者：
Wong, Wing H.
DOI：
10.1016/j.bbamcr.2011.06.015
发表时间：
2011-10-01
影响因子：
5.1
作者：
Katsarou, Konstantina;Tsitoura, Panagiota;Georgopoulou, Urania
通讯作者：
Georgopoulou, Urania