Exacerbation of allergic inflammation in mice exposed to diesel exhaust particles prior to viral infection.
Exacerbation of allergic inflammation in mice exposed to diesel exhaust particles prior to viral infection.
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DOI：
10.1186/1743-8977-6-22
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发表时间：
2009-08-14
影响因子：
10
通讯作者：
Tilley SL
中科院分区：
文献类型：
--
作者：
Jaspers I;Sheridan PA;Zhang W;Brighton LE;Chason KD;Hua X;Tilley SL
病毒感染和暴露于氧化性空气污染物是哮喘恶化的两个最重要的诱因。我们先前的研究已经证明，暴露于柴油机废气增加了体外上皮细胞和体内小鼠对流感病毒感染的易感性。因此，我们研究了在过敏性哮喘的背景下，暴露于氧化剂空气污染物是否会增加对呼吸道病毒感染的易感性，从而导致病毒诱导的哮喘加重。将卵清蛋白致敏（OVA）的雄性C57 BL/6小鼠用柴油机排气颗粒（DEP）或盐水滴注，24小时后用流感A/PR/8感染。感染后24小时处死动物，并分析肺损伤、过敏性炎症和促炎细胞因子产生的标志物。暴露于DEP或单独感染流感对损伤或过敏性炎症的标志物没有显著影响。然而，暴露于DEP并随后感染流感的OVA致敏小鼠在肺灌洗液和组织中显示嗜酸性粒细胞水平增加。此外，在感染流感前暴露于DEP的OVA致敏小鼠中，Th 2型细胞因子（如IL-4和IL-13）和嗜酸性粒细胞趋化性标志物（如CCL 11和CCR 3）增加。这些小鼠还显示肺匀浆中IL-1α水平升高，但IL-10、RANTES和MCP-1水平未升高。这些数据表明，在过敏性哮喘的背景下，暴露于柴油机废气可以增强病毒诱导的过敏性炎症的恶化。
Viral infections and exposure to oxidant air pollutants are two of the most important inducers of asthma exacerbation. Our previous studies have demonstrated that exposure to diesel exhaust increases the susceptibility to influenza virus infections both in epithelial cells in vitro and in mice in vivo. Therefore, we examined whether in the setting of allergic asthma, exposure to oxidant air pollutants enhances the susceptibility to respiratory virus infections, which in turn leads to increased virus-induced exacerbation of asthma. Ovalbumin-sensitized (OVA) male C57BL/6 mice were instilled with diesel exhaust particles (DEP) or saline and 24 hours later infected with influenza A/PR/8. Animals were sacrificed 24 hours post-infection and analyzed for markers of lung injury, allergic inflammation, and pro-inflammatory cytokine production. Exposure to DEP or infection with influenza alone had no significant effects on markers of injury or allergic inflammation. However, OVA-sensitized mice that were exposed to DEP and subsequently infected with influenza showed increased levels of eosinophils in lung lavage and tissue. In addition Th2-type cytokines, such as IL-4 and IL-13, and markers of eosinophil chemotaxis, such as CCL11 and CCR3, were increased in OVA-sensitized mice exposed to DEP prior to infection with influenza. These mice also showed increased levels of IL-1α, but not IL-10, RANTES, and MCP-1 in lung homogenates. These data suggest that in the setting of allergic asthma, exposure to diesel exhaust could enhance virus-induced exacerbation of allergic inflammation.
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影响因子：
10.4
作者：
Singh P;DeMarini DM;Dick CA;Tabor DG;Ryan JV;Linak WP;Kobayashi T;Gilmour MI
通讯作者：
Gilmour MI
影响因子：
4.5
作者：
Ichinose, T;Takano, H;Shibamoto, T
通讯作者：
Shibamoto, T
DOI：
10.1165/ajrcmb.21.3.f160
发表时间：
1999-09-01
影响因子：
6.4
作者：
Rothenberg, ME
通讯作者：
Rothenberg, ME
影响因子：
4.5
作者：
Ichinose, T;Takano, H;Sagai, M
通讯作者：
Sagai, M
影响因子：
5.5
作者：
FARAGMAHMOD, FI;WYDE, PR;SIX, HR
通讯作者：
SIX, HR