Lena P, Freyria A M, Lyon M, Cadoré J L, Guiguen F, Greenland T, Belleville J, Cordier G, Mornex J F
Laboratoire d'Immunologie et de Biologie pulmonaire, INSERM/CJF 93-08, Hôpital Louis Pradel, Lyon, France.
Res Virol. 1994 May-Aug;145(3-4):209-14. doi: 10.1016/s0923-2516(07)80024-0.
To link ovine lentivirus infection to lung tissue damage, we studied the procoagulant response in alveolar macrophages from experimentally infected lambs and in in vitro infected alveolar macrophages. We cloned ovine tissue factor cDNA and analysed its in vitro expression by Northern blotting. Visna-maedi virus induced tissue factor mRNA. In order to correlate this mRNA induction with its cellular function, we analysed macrophage procoagulant activity after in vitro and in vivo infection. The procoagulant activity was increased by interaction with the virus in both cases. Thus, visna-maedi virus-induced expression of tissue factor mRNA was associated with enhanced macrophage procoagulant activity. These findings indicate an active role of alveolar macrophages in the pathogenesis of these inflammatory lung lesions.
为了将绵羊慢病毒感染与肺组织损伤联系起来，我们研究了来自实验感染羔羊的肺泡巨噬细胞以及体外感染的肺泡巨噬细胞中的促凝反应。我们克隆了绵羊组织因子cDNA，并通过Northern印迹分析其体外表达。维斯纳-梅迪病毒诱导组织因子mRNA表达。为了将这种mRNA诱导与其细胞功能相关联，我们分析了体外和体内感染后巨噬细胞的促凝活性。在这两种情况下，与病毒相互作用后促凝活性均增加。因此，维斯纳-梅迪病毒诱导的组织因子mRNA表达与巨噬细胞促凝活性增强有关。这些发现表明肺泡巨噬细胞在这些炎症性肺损伤的发病机制中起积极作用。
