Rodgers B C, Mims C A
Infect Immun. 1982 Jun;36(3):1154-9. doi: 10.1128/iai.36.3.1154-1159.1982.
Lung macrophages from uninfected CD1 mice support the replication of influenza viruses (H1N1 and H0N1), but the cells from influenza-infected mice do not. The possible mechanisms of this resistance were investigated. Murine macrophages were "activated" in vitro with lipopolysaccharide and lymphokines, and in both cases activation was associated with resistance of cells to infection with influenza virus. Exposure of alveolar macrophages in vitro to 500 U of purified type I interferon per ml enhanced cell spreading and Fc receptor-mediated phagocytosis, suggesting macrophage activation, and protected the cells against infection with influenza virus. Alveolar macrophages were also protected by a soluble factor in the bronchoalveolar washings from influenza-infected mice. This effect was not virus specific and was abolished by anti-interferon serum.
未感染的CD1小鼠的肺巨噬细胞能支持流感病毒(H1N1和H0N1)的复制,但来自流感感染小鼠的细胞则不能。对这种抗性的可能机制进行了研究。用脂多糖和淋巴因子在体外“激活”小鼠巨噬细胞,在这两种情况下,激活都与细胞对流感病毒感染的抗性有关。体外将肺泡巨噬细胞暴露于每毫升500单位的纯化I型干扰素中,可增强细胞铺展和Fc受体介导的吞噬作用,提示巨噬细胞被激活,并保护细胞免受流感病毒感染。来自流感感染小鼠的支气管肺泡灌洗液中的一种可溶性因子也能保护肺泡巨噬细胞。这种作用不是病毒特异性的,且可被抗干扰素血清消除。