Ratcliffe D R, Nolin S L, Cramer E B
Department of Anatomy and Cell Biology, State University of New York Health Science Center, Brooklyn 11203.
Blood. 1988 Jul;72(1):142-9.
An in vitro model system was used to study the early neutrophil response to influenza-infected epithelia. In the absence of serum, neutrophil adherence to influenza-infected confluent monolayers of Madin-Darby canine kidney epithelial cells (MDCK) was approximately 590 times greater than neutrophil binding to control cultures. The leukocytes bound specifically to virus-infected cells. Neutrophil adherence to influenza-infected MDCK cells was monitored during the course of one replication cycle, and binding began at a time (4.5 hours) that coincided with viral protein insertion in the apical cell membrane. Ultrastructural examination at 4.5 hours showed that greater than 90% of the neutrophils adhered to the epithelial cell membrane in the absence of budding virus and, at 6.5 hours, 100% of the neutrophils adhered to the epithelium with emerging virions. The number of neutrophils bound to influenza-infected MDCK cells was not affected by the presence or absence of calcium or magnesium but did depend on the amount of viral inoculum and on the temperature of the culture. In direct contrast to hemadsorption of RBCs, neutrophil binding to influenza-infected MDCK cells was 100% greater at 37 degrees C than at 4 degrees C. The neutrophil surface molecules that bound influenza virus appeared to become functionally polarized because the adherence of neutrophils to budding influenza virus or to a virus-coated surface inhibited the neutrophils from binding additional influenza virus to their nonadherent surface.
利用体外模型系统研究中性粒细胞对流感感染上皮细胞的早期反应。在无血清条件下,中性粒细胞对流感感染的汇合单层马-达二氏犬肾上皮细胞(MDCK)的黏附比其对对照培养物的结合高约590倍。白细胞特异性结合病毒感染的细胞。在一个复制周期过程中监测中性粒细胞对流感感染的MDCK细胞的黏附情况,结合在与病毒蛋白插入顶细胞膜的时间(4.5小时)一致时开始。4.5小时的超微结构检查显示,在无出芽病毒的情况下,超过90%的中性粒细胞黏附于上皮细胞膜,而在6.5小时时,100%的中性粒细胞黏附于有新出现病毒粒子的上皮细胞。黏附于流感感染的MDCK细胞的中性粒细胞数量不受钙或镁存在与否的影响,但确实取决于病毒接种量和培养温度。与红细胞的血细胞吸附形成直接对比的是,中性粒细胞在37℃时对流感感染的MDCK细胞的结合比在4℃时高100%。结合流感病毒的中性粒细胞表面分子似乎发生了功能极化,因为中性粒细胞对出芽流感病毒或病毒包被表面的黏附抑制了中性粒细胞将额外的流感病毒结合到其未黏附表面。