Viral infection of bovine bronchial epithelial cells induces increased neutrophil chemotactic activity and neutrophil adhesion.

Viral infection of bovine bronchial epithelial cells induces increased neutrophil chemotactic activity and neutrophil adhesion.
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牛支气管上皮细胞的病毒感染诱导中性粒细胞趋化活性和中性粒细胞粘附增加。

DOI:
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发表时间:
1993
期刊:
影响因子:
6
通讯作者:
J. Spurzem
J. Spurzem
中科院分区:
医学2区
文献类型:
--
作者:
M. Raz;R. Robbins;C. Kelling;L. Stine;G. Leikauf;S. Rennard;J. Spurzem

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1. 继发于病毒感染的急性支气管炎与中性粒细胞的涌入有关。我们假设支气管上皮细胞能够释放中性粒细胞趋化活性以响应病毒感染。2. 为了验证这一假设,用牛呼吸道病原体牛疱疹病毒-1接种了原代培养的牛支气管上皮细胞。3. 从接种细胞中收集的上清液,在毒性迹象出现之前,通过盲孔室中性粒细胞趋化试验显示出显著的中性粒细胞趋化活性。脂氧合酶抑制剂显著降低接种牛疱疹病毒-1后中性粒细胞趋化活性的释放量。反相高效液相色谱法分析细胞上清液中花生四烯酸代谢物,证实释放出一种强效的中性粒细胞化学引诱剂白三烯B4。4. 我们还证实,中性粒细胞对接种过的牛疱疹病毒-1的支气管上皮细胞的粘附增强,部分是由中性粒细胞整合素LFA-1介导的。5. 因此,受病毒感染的气道上皮细胞释放白细胞化学引诱剂,从而产生粘附相互作用,这些功能可能在对病毒感染的炎症急性反应中很重要。
1. Acute bronchitis secondary to viral infection is associated with an influx of neutrophils. We hypothesized that bronchial epithelial cells are capable of releasing neutrophil chemotactic activity in response to viral infection. 2. To test this hypothesis, primary cultures of bovine bronchial epithelial cells were inoculated with a bovine respiratory pathogen, bovine herpes virus-1. 3. Supernatants collected from inoculated cells, before signs of toxicity, demonstrated significant neutrophil chemotactic activity using a blind well chamber neutrophil chemotaxis assay. Lipoxygenase inhibitors markedly reduced the amount of neutrophil chemotactic activity released after bovine herpes virus-1 inoculation. Analysis of arachidonic acid metabolites in cell supernatants by reverse-phase h.p.l.c. confirmed that leukotriene B4, a potent neutrophil chemoattractant, was released. 4. We also confirmed that adhesion of neutrophils to bovine herpes virus-1-inoculated bronchial epithelial cells was increased and mediated in part by the neutrophil integrin, LFA-1. 5. Thus, virally infected airway epithelial cells release leucocyte chemoattractants and hence adhesive interactions, functions that are likely to be important in the inflammatory acute response to viral infection.