Activation of interleukin-32 pro-inflammatory pathway in response to influenza A virus infection.
Activation of interleukin-32 pro-inflammatory pathway in response to influenza A virus infection.
复制标题
响应甲型流感病毒感染而激活白细胞介素 32 促炎途径。
DOI：
10.1371/journal.pone.0001985
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发表时间：
2008-04-16
期刊：
影响因子：
3.7
通讯作者：
Zhu, Ying
中科院分区：
文献类型：
--
作者：
Li, Wei;Liu, Yan;Mukhtar, Muhammad Mahmood;Gong, Rui;Pan, Ying;Rasool, Sahibzada T.;Gao, Yecheng;Kang, Lei;Hao, Qian;Peng, Guiqing;Chen, Yanni;Chen, Xin;Wu, Jianguo;Zhu, Ying
白细胞介素（IL）-32是最近描述的促炎细胞因子，其已被报道在培养细胞中由细菌处理诱导。关于外源性病原体感染在人类个体中产生IL-32的情况知之甚少。在这项研究中，我们发现IL-32水平在108例甲型流感病毒感染患者的血清样品中比115名健康人的血清样品中增加了58.2%。另一种促炎因子环氧合酶（考克斯）-2相关的前列腺素E2也上调了2.7倍。在甲型流感病毒感染的A549人肺上皮细胞中IL-32的表达被选择性考克斯-2抑制剂NS 398或已知的抗炎药阿司匹林阻断，表明IL-32在炎症级联中通过考克斯-2诱导。有趣的是，我们发现流感病毒感染激活的考克斯-2相关PGE 2的产生被IL-32过表达显著抑制，但被IL-32特异性siRNA增加，这表明IL-32和考克斯-2之间存在反馈机制。在炎症级联反应中，甲型流感病毒感染通过考克斯-2诱导IL-32。我们的研究结果表明，IL-32是一个潜在的目标，抗炎药物筛选。
Interleukin (IL)-32 is a recently described pro-inflammatory cytokine that has been reported to be induced by bacteria treatment in culture cells. Little is known about IL-32 production by exogenous pathogens infection in human individuals. In this study, we found that IL-32 level was increased by 58.2% in the serum samples from a cohort of 108 patients infected by influenza A virus comparing to that of 115 healthy individuals. Another pro-inflammatory factor cyclooxygenase (COX)-2-associated prostaglandin E2 was also upregulated by 2.7-fold. Expression of IL-32 in influenza A virus infected A549 human lung epithelial cells was blocked by either selective COX-2 inhibitor NS398 or Aspirin, a known anti-inflammatory drug, indicating IL-32 was induced through COX-2 in the inflammatory cascade. Interestingly, we found that COX-2-associate PGE2 production activated by influenza virus infection was significantly suppressed by over-expression of IL-32 but increased by IL-32-specific siRNA, suggesting there was a feedback mechanism between IL-32 and COX-2. IL-32 is induced by influenza A virus infection via COX-2 in the inflammatory cascade. Our results provide that IL-32 is a potential target for anti-inflammatory medicine screening.
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影响因子：
15.9
作者：
Lara-Pezzi, E;Gómez-Gaviro, MV;López-Cabrera, M
通讯作者：
López-Cabrera, M
影响因子：
4.8
作者：
Liu, Mo;Yang, Yongbo;Zhu, Ying
通讯作者：
Zhu, Ying
DOI：
10.1073/pnas.0511206103
发表时间：
2006-02-28
影响因子：
11.1
作者：
Novick, D;Rubinstein, M;Kim, SH
通讯作者：
Kim, SH
影响因子：
4.8
作者：
Deng, WG;Zhu, Y;Wu, KK
通讯作者：
Wu, KK
影响因子：
4.8
作者：
Eliopoulos, AG;Gallagher, NJ;Young, LS
通讯作者：
Young, LS