To determine the nature of the interaction between viruses and eosinophils, normodense eosinophils were separated from the blood of healthy volunteers and incubated in vitro with respiratory syncytial virus (RSV). After incubation for 2 h with the virus, 29.5 ± 15.8% of the eosinophils demonstrated specific binding of the virus to the cell membrane, as detected by fluorescent staining with an anti-RSV MAb. Superoxide production and leu-kotriene C4 release were measured as determinants of cell activation. Using a cytochrome c reduction assay, superoxide could be detected in the supernatant 30 min after exposure to RSV. Maximal release was reached at 3 h postexposure (5.88 ± 2.19 nmol cytochrome c reduction/5 X 105 cells). The virus-induced superoxide generation varied in magnitude among different subjects and ranged from 0.6 to 11.5 nmol cytochrome c reduction/5 x 10s cells. RSV also appeared to prime eosinophils to the effects of other known cell activators, as demonstrated by an increase in superoxide production upon subsequent stimulation of RSV-primed cells with phorbol-12-myristate-13-acetate (21.4 ± 5.8 versus 9.4 ± 2.7 nmol cytochrome c reduction/ 5 x 105 cells for primed and unprimed cells, respectively) (p < 0.04). RSV did not directly induce leukotriene C4release from the eosinophils but primed the cells to exhibit a more vigorous response on subsequent challenge with the calcium ionophore A23187 (9.16 ± 1.04 versus 4.2 ±1.3 ng leukotriene C/l x 106 cells) (p < 0.005). These findings indicate that RSV can activate or prime eosinophils to release various inflammatory mediators. Such virus-induced effects on inflammatory cells may play a role in the pathogenesis of RSV bronchiolitis and may also be critical for the development of persistent airway hyperreactivity after viral infections.
ASJC Scopus subject areas
- Pediatrics, Perinatology, and Child Health