Viral infection modulates expression of hypersensitivity pneumonitis.

Viral infection modulates expression of hypersensitivity pneumonitis.
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DOI:
10.4049/jimmunol.162.12.7397
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发表时间:
1999-06
影响因子:
4.4
通讯作者:
Gunnar Gudmundsson;M. Monick;G. Hunninghake
Gunnar Gudmundsson;M. Monick;G. Hunninghake
中科院分区:
医学2区
文献类型:
--
作者:
Gunnar Gudmundsson;M. Monick;G. Hunninghake

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过敏性肺炎(HP)是一种肉芽肿性炎症性肺部疾病,由吸入有机AGs引起,最常见的是导致农民肺部疾病的嗜热放线菌。对Ag的早期反应是肺内中性粒细胞增加,而晚期反应是典型的Th1型肉芽肿性疾病。许多罹患疾病的患者报告说,最近发生了一次病毒性呼吸道感染。这些研究是为了确定病毒是否可以增强幽门螺杆菌的炎症反应。将C57BL/6小鼠暴露于嗜热菌直立型糖多孢菌(SR)中,每周连续3d,共3wk。一些小鼠在感染呼吸道合胞病毒(RSV)后2周暴露于SR,而另一些小鼠在单独暴露于生理盐水或热灭活RSV后暴露于SR。SR处理的小鼠出现典型的早期中性粒细胞反应和晚期肉芽肿性炎症反应。在晚期反应中,干扰素-γ和IL-2基因的表达也有上调。这些反应被最近的RSV感染增强,但不被热灭活的RSV增强。既往感染RSV的小鼠对SR的早期中性粒细胞反应也更强,支气管肺泡灌洗液中巨噬细胞炎症蛋白-2(MIP-2,相当于小鼠的IL-8)释放增加。这些研究表明,病毒感染可以增强幽门螺杆菌的早期和晚期炎症反应。
Hypersensitivity pneumonitis (HP) is a granulomatous, inflammatory lung disease caused by inhalation of organic Ags, most commonly thermophilic actinomycetes that cause farmer's lung disease. The early response to Ag is an increase in neutrophils in the lung, whereas the late response is a typical Th1-type granulomatous disease. Many patients who develop disease report a recent viral respiratory infection. These studies were undertaken to determine whether viruses can augment the inflammatory responses in HP. C57BL/6 mice were exposed to the thermophilic bacteria Saccharopolyspora rectivirgula (SR) for 3 consecutive days per wk for 3 wk. Some mice were exposed to SR at 2 wk after infection with respiratory syncytial virus (RSV), whereas others were exposed to SR after exposure to saline alone or to heat-inactivated RSV. SR-treated mice developed a typical, early neutrophil response and a late granulomatous inflammatory response. Up-regulation of IFN-gamma and IL-2 gene expression was also found during the late response. These responses were augmented by recent RSV infection but not by heat-inactivated RSV. Mice with a previous RSV infection also had a greater early neutrophil response to SR, with increased macrophage inflammatory protein-2 (MIP-2, murine equivalent of IL-8) release in bronchoalveolar lavage fluid. These studies suggest that viral infection can augment both the early and late inflammatory responses in HP.