Singleton Helen, Graham Simon P, Frossard Jean-Pierre, Bodman-Smith Katherine B, Steinbach Falko
Virology Department, Animal and Plant Health Agency, Woodham Lane, New Haw, Addlestone, KT15 3NB Surrey, United Kingdom; Faculty of Health and Medical Sciences, University of Surrey, Guildford GU2 7XH, United Kingdom.
Virology Department, Animal and Plant Health Agency, Woodham Lane, New Haw, Addlestone, KT15 3NB Surrey, United Kingdom.
Virology. 2018 Apr;517:199-207. doi: 10.1016/j.virol.2018.02.017. Epub 2018 Mar 2.
Monocytes are considered refractory to porcine reproductive and respiratory syndrome virus type 1 (PRRSV-1) infection. However, monocytes are only short-lived in blood, being able to differentiate into macrophages and dendritic cells (DC). It was therefore merited to revisit PRRSV-1 interaction with monocytes, particularly those treated with cytokines influencing monocyte biology. Thus, several factors were screened, particularly those modulating monocyte differentiation and expression of putative PRRSV-1 receptors (CD169 and CD163). M-CSF, known to stimulate macrophage differentiation, did not increase their susceptibility to PRRSV-1. Nor did GM-CSF or IL-4, known drivers for monocyte-derived DC (MoDC) differentiation. In contrast, monocyte treatment with IL-10 or the corticosteroid, dexamethasone, known to be potent suppressors of monocyte differentiation, was correlated with increased susceptibility to PRRSV-1 infection. While this effect was strongly correlated to CD163 and CD169 expression, our data suggest that receptor expression is not the only factor driving successful infection of PPRSV-1 in monocytes.
单核细胞被认为对1型猪繁殖与呼吸综合征病毒（PRRSV - 1）感染具有抗性。然而，单核细胞在血液中寿命短暂，能够分化为巨噬细胞和树突状细胞（DC）。因此，有必要重新审视PRRSV - 1与单核细胞的相互作用，特别是那些受到影响单核细胞生物学的细胞因子处理的单核细胞。于是，筛选了几种因子，尤其是那些调节单核细胞分化和假定的PRRSV - 1受体（CD169和CD163）表达的因子。已知刺激巨噬细胞分化的巨噬细胞集落刺激因子（M - CSF）并未增加其对PRRSV - 1的易感性。已知驱动单核细胞衍生DC（MoDC）分化的粒细胞 - 巨噬细胞集落刺激因子（GM - CSF）或白细胞介素 - 4（IL - 4）也没有增加其易感性。相反，用白细胞介素 - 10或皮质类固醇地塞米松处理单核细胞，已知它们是单核细胞分化的有效抑制剂，这与PRRSV - 1感染易感性增加相关。虽然这种效应与CD163和CD169表达密切相关，但我们的数据表明受体表达并非驱动PRRSV - 1成功感染单核细胞的唯一因素。
