Kazhdan M, White M R, Tauber A I, Hartshorn K L
Department of Medicine, Boston University School of Medicine, Massachusetts 02118.
J Leukoc Biol. 1994 Jul;56(1):59-64. doi: 10.1002/jlb.56.1.59.
We have studied in detail the in vitro interactions of influenza A viruses (IAVs) with human neutrophils to clarify why these cells become dysfunctional during IAV infection. Unosponized IAV elicited a respiratory burst response in neutrophils which, like that triggered by formylmethionyl-leucyl-phenylalanine (fMLP), involved mediation of signal-transducing GTP-binding proteins and tyrosine kinase activation. The IAV-induced response differed from that provoked by fMLP in that H2O2 was produced without concomitant O2- release. IAV also did not cause extracellular release of granule enzymes in cytochalasin B-treated neutrophils. Using chemiluminescence assays, the respiratory burst response to IAV was found to occur at an intracellular location. These findings may, in part, explain the anomalous nature of the respiratory burst response elicited by IAV and suggest strategies for determining the mechanism of IAV-induced neutrophil deactivation.
我们已经详细研究了甲型流感病毒（IAV）与人类中性粒细胞的体外相互作用，以阐明这些细胞在IAV感染期间功能失调的原因。未调理的IAV在中性粒细胞中引发了呼吸爆发反应，该反应与由甲酰甲硫氨酰 - 亮氨酰 - 苯丙氨酸（fMLP）触发的反应类似，涉及信号转导GTP结合蛋白的介导和酪氨酸激酶激活。IAV诱导的反应与fMLP引发的反应不同之处在于，产生H2O2时没有伴随O2-释放。IAV也不会导致细胞松弛素B处理的中性粒细胞中颗粒酶的细胞外释放。使用化学发光测定法，发现对IAV的呼吸爆发反应发生在细胞内位置。这些发现可能部分解释了IAV引发的呼吸爆发反应的异常性质，并为确定IAV诱导中性粒细胞失活的机制提供了策略。
