Respiratory Syncytial Virus-Infected Pulmonary Epithelial Cells Induce Eosinophil Degranulation by a CD18-Mediated Mechanism

摘要: Respiratory syncytial virus (RSV)-induced bronchiolitis in infants is characterized by wheezing, respiratory distress, and the histologic findings of necrosis sloughing airway epithelium. High concentrations eosinophil cationic protein (ECP), a cytotoxic contained granules eosinophils, have been found airways RSV-infected infants. The mechanisms degranulation vivo remain largely unknown. Since epithelial cells are rich source cytokines with eosinophil-activating properties, our studies were designed to mimic vitro interaction between RSV, pulmonary (A549), eosinophils mucosa. We report this work that, absence cells, neither form purified virions, nor UV-irradiated culture supernatant (RSV-CM) induced degranulation. On other hand, released significant amount ECP when cultured A549 cells. Uninfected which failed induce degranulation, equally effective triggering release if they presence RSV-CM. Although RSV-CM up-regulation β 2 integrin CD11b on expression ICAM-1 was inhibited significantly anti-CD18 mAb, but not anti-ICAM-1 mAb. These results suggest novel mechanism viruses may trigger detrimental granule proteins