Influenza virus A stimulates expression of eotaxin by nasal epithelial cells
Influenza virus A stimulates expression of eotaxin by nasal epithelial cells
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DOI：
10.1046/j.1365-2222.2001.01103.x
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发表时间：
2001-06-01
影响因子：
6.1
通讯作者：
Adachi, M
中科院分区：
文献类型：
--
作者：
Kawaguchi, M;Kokubu, F;Adachi, M
研究背景呼吸道病毒是引起气道炎症最常见的原因之一，但其致病机制尚不清楚。嗜酸性粒细胞趋化因子是一种有效的嗜酸性粒细胞化学引诱物，是C-C趋化因子受体3（CCR 3）的选择性激动剂。尽管最近已经证明上皮细胞在体内和体外都表达嗜酸性粒细胞趋化因子，目的探讨病毒感染对鼻黏膜上皮细胞中嗜酸性粒细胞趋化因子（eotaxin，Eotaxin）表达的影响，并分析病毒感染对鼻黏膜上皮细胞中Eotaxin表达的影响。息肉感染流感病毒A（亚型H3 N2）。在感染后8、24和48 h收集细胞和上清液。通过RT-PCR分析Eotaxin mRNA。通过酶联免疫吸附测定法分析上清液中的嗜酸性粒细胞趋化因子浓度。我们还研究了阻断分析干预的促炎细胞因子，TNF-α和IL-1 β诱导的流感病毒。结果表明，eotaxin在未感染的细胞组成型表达，但在感染的细胞中的mRNA和蛋白质水平上调。使用抗-TNF-α和抗-IL-1 β抗体的阻断实验显示这些试剂对嗜酸性粒细胞趋化因子水平没有影响。结论A型流感病毒感染鼻黏膜上皮细胞后，Eotaxin的表达增加，可能通过诱导Eotaxin的表达而在气道炎症的发病中发挥重要作用。
Background Respiratory virus is one of the most common causes of airway inflammation, but its pathogenic mechanisms are not well understood. Eotaxin is a potent eosinophil chemoattractant and is a selective agonist for C-C chemokine receptor 3 (CCR3). Although it has recently been demonstrated that epithelial cells express eotaxin, both in vivo and in vitro, there are few data concerning the expression in viral infection.Objects We hypothesized that eotaxin may play an important role in attracting inflammatory cells into the airway after viral infection and analysed whether viral infection induces eotaxin in nasal epithelial cells in vitro.Methods Nasal epithelial cells obtained from polypectomy for nasal polyp were infected with influenza virus A (subtype H3N2). The cells and supernatants were collected 8, 24 and 48 h after infection. Eotaxin mRNA was analysed by RT-PCR. Eotaxin concentration in the supernatants was analysed by enzyme-linked immunosorbent assay. We also examined a blocking assay to analyse the intervention of pro-inflammatory cytokines, TNF-alpha and IL-1 beta in eotaxin production induced by influenza virus.Results The results showed that eotaxin was expressed constitutively in uninfected cells, but was up-regulated for both mRNA and protein levels in infected cells. Blocking experiments using anti-TNF-alpha and anti-IL-1 beta antibodies showed no effects of these agents on the level of eotaxin. In addition, UV-inactivated virus did not enhance the expression of eotaxin.Conclusions These results suggest that influenza virus A infection in nasal epithelial cells stimulates the expression of eotaxin, and may play an important role in the pathogenesis of airway inflammation by inducing eotaxin.