Respiratory Syncytial Virus (RSV) infection inhibits lung eosinophilia, but induces profound eosinophil degranulation in allergic mice

呼吸道合胞病毒诱导的婴儿毛细支气管炎的特点是鼻腔和气管抽吸物中有高浓度的嗜酸性粒细胞衍生蛋白，包括ECP、MBP和EDN。然而，证明呼吸道合胞病毒感染的婴儿的呼吸道粘膜或分泌物中是否存在嗜酸性粒细胞的尝试一直没有成功。我们使用了BALB/c小鼠的肺嗜酸性粒细胞增多症(OVA诱导)模型。卵子致敏、激发(反复雾化卵清蛋白)小鼠感染RSV或假接种RSV，分别于接种RSV或假接种后第1天行支气管肺泡灌洗(BAL)细胞分类计数。肺泡灌洗液中嗜酸性粒细胞过氧化物酶活性通过比色法测定。呼吸道合胞病毒感染卵清蛋白攻击组小鼠肺泡灌洗液中嗜酸粒细胞的数量(1.3x10^5/ml)显著低于假感染卵清蛋白攻击组小鼠(4.0x10^5/m1)(p&lt；0.001)。卵子攻击、假感染的小鼠没有嗜酸性粒细胞脱颗粒的证据，因为在BAL液中没有检测到EPO活性。另一方面，OVA攻击、RSV感染的小鼠在BAL液中有高水平的EPO活性(p&lt；0.01)。这些发现表明，RSV感染和嗜酸性粒细胞的迁移和激活途径之间存在复杂的相互作用，可能影响特应性和非特应性个体对呼吸道病毒感染的反应。

RSV-induced bronchiolitis in infants is characterized by high concentrations of eosinophil-derived proteins, including ECP, MBP, and EDN, in nasal and tracheal aspirates. However, attempts to demonstrate the presence of eosinophils in airway mucosa or secretions of infants with RSV infections have been unsuccessful.A BALB/c mouse model of lung eosinophilia (OVA-induced) was used. OVA-sensitized, challenged (by repeated OVA nebulization) mice were infected with RSV or sham-inoculated and differential cell counts were performed in cells recovered by bronchoalveolar lavage (BAL) at day 1 after RSV or sham inoculation. Eosinophil peroxidase (EPO) activity in the BAL fluid was measured by a specific colorimetric assay.A significant reduction in the number of BAL eosinophils was observed in RSV-infected OVA-challenged mice (1.3×10^5/ml) compared with sham-infected, OVA-challenged mice (4.0×10^5/m1) (p<0.001). OVA-challenged, sham infected mice had no evidence of eosinophil degranulation, as no detectable EPO activity was present in the BAL fluid. On the other hand, OVA-challenged, RSV-infected mice had high levels of EPO activity in BAL fluid (p<0.01).These findings suggest the existence of a complex interplay between RSV infection and the migratory and activation pathways of eosinophils that may affect the response of atopic as well as non-atopic individuals to respiratory viral infections.